Connective Tissue Growth Factor
Intercellular Signaling Peptides and Proteins
Nephroblastoma Overexpressed Protein
Transforming Growth Factor beta
Transforming Growth Factor beta1
Connective Tissue Diseases
Cysteine-Rich Protein 61
Connective Tissue Cells
CCN Intercellular Signaling Proteins
Collagen Type I
Gene Expression Regulation
Mixed Connective Tissue Disease
Reverse Transcriptase Polymerase Chain Reaction
Vascular Endothelial Growth Factor A
Extracellular Matrix Proteins
Transforming Growth Factor beta2
Epidermal Growth Factor
Collagen Type III
Receptors, Transforming Growth Factor beta
Disease Models, Animal
Receptor, Epidermal Growth Factor
Insulin-Like Growth Factor Binding Proteins
Collagen Type IV
Hepatic Stellate Cells
Diabetes Mellitus, Experimental
In Situ Hybridization
Focal Epithelial Hyperplasia
Fibroblast Growth Factor 2
RNA, Small Interfering
Insulin-Like Growth Factor I
Promoter Regions, Genetic
Hepatocyte Growth Factor
Platelet-Derived Growth Factor
rhoA GTP-Binding Protein
Culture Media, Conditioned
Fibroblast Growth Factors
Transforming Growth Factors
MAP Kinase Signaling System
Enzyme-Linked Immunosorbent Assay
Molecular Sequence Data
Endothelial Growth Factors
Extracellular Signal-Regulated MAP Kinases
Transforming Growth Factor alpha
Kidney Tubules, Proximal
Mitogen-Activated Protein Kinase 3
Gene Expression Profiling
Matrix Metalloproteinase 2
Nerve Growth Factors
Vascular Endothelial Growth Factors
Mitogen-Activated Protein Kinase 1
Dose-Response Relationship, Drug
NIH 3T3 Cells
Expression and differential regulation of connective tissue growth factor in pancreatic cancer cells. (1/856)CTGF is an immediate early growth responsive gene that has been shown to be a downstream mediator of TGFbeta actions in fibroblasts and vascular endothelial cells. In the present study hCTGF was isolated as immediate early target gene of EGF/TGFalpha in human pancreatic cancer cells by suppression hybridization. CTGF transcripts were found in 13/15 pancreatic cancer cell lines incubated with 10% serum. In 3/7 pancreatic cancer cell lines EGF/TGFalpha induced a significant rise of CTGF transcript levels peaking 1-2 h after the start of treatment. TGFbeta increased CTGF transcript levels in 2/7 pancreatic cancer cell lines after 4 h of treatment and this elevation was sustained after 24 h. Only treatment with TGFbeta was accompanied by a parallel induction of collagen type I transcription. 15/19 human pancreatic cancer tissues were shown to overexpress high levels of CTGF transcripts. CTGF transcript levels in pancreatic cancer tissues and nude mouse xenograft tumors showed a good correlation to the degree of fibrosis. In situ hybridization and the nude mouse experiments revealed that in pancreatic cancer tissues, fibroblasts are the predominant site of CTGF transcription, whereas the tumor cells appear to contribute to a lesser extent. We conclude that CTGF may be of paramount importance for the development of the characteristic desmoplastic reaction in pancreatic cancer tissues. (+info)
Suppression subtractive hybridization identifies high glucose levels as a stimulus for expression of connective tissue growth factor and other genes in human mesangial cells. (2/856)Accumulation of mesangial matrix is a pivotal event in the pathophysiology of diabetic nephropathy. The molecular triggers for matrix production are still being defined. Here, suppression subtractive hybridization identified 15 genes differentially induced when primary human mesangial cells are exposed to high glucose (30 mM versus 5 mM) in vitro. These genes included (a) known regulators of mesangial cell activation in diabetic nephropathy (fibronectin, caldesmon, thrombospondin, and plasminogen activator inhibitor-1), (b) novel genes, and (c) known genes whose induction by high glucose has not been reported. Prominent among the latter were genes encoding cytoskeleton-associated proteins and connective tissue growth factor (CTGF), a modulator of fibroblast matrix production. In parallel experiments, elevated CTGF mRNA levels were demonstrated in glomeruli of rats with streptozotocin-induced diabetic nephropathy. Mannitol provoked less mesangial cell CTGF expression in vitro than high glucose, excluding hyperosmolality as the key stimulus. The addition of recombinant CTGF to cultured mesangial cells enhanced expression of extracellular matrix proteins. High glucose stimulated expression of transforming growth factor beta1 (TGF-beta1), and addition of TGF-beta1 to mesangial cells triggered CTGF expression. CTGF expression induced by high glucose was partially suppressed by anti-TGF-beta1 antibody and by the protein kinase C inhibitor GF 109203X. Together, these data suggest that 1) high glucose stimulates mesangial CTGF expression by TGFbeta1-dependent and protein kinase C dependent pathways, and 2) CTGF may be a mediator of TGFbeta1-driven matrix production within a diabetic milieu. (+info)
Fisp12/mouse connective tissue growth factor mediates endothelial cell adhesion and migration through integrin alphavbeta3, promotes endothelial cell survival, and induces angiogenesis in vivo. (3/856)Fisp12 was first identified as a secreted protein encoded by a growth factor-inducible immediate-early gene in mouse fibroblasts, whereas its human ortholog, CTGF (connective tissue growth factor), was identified as a mitogenic activity in conditioned media of human umbilical vein endothelial cells. Fisp12/CTGF is a member of a family of secreted proteins that includes CYR61, Nov, Elm-1, Cop-1/WISP-2, and WISP-3. Fisp12/CTGF has been shown to promote cell adhesion and mitogenesis in both fibroblasts and endothelial cells and to stimulate cell migration in fibroblasts. These findings, together with the localization of Fisp12/CTGF in angiogenic tissues, as well as in atherosclerotic plaques, suggest a possible role for Fisp12/CTGF in the regulation of vessel growth during development, wound healing, and vascular disease. In this study, we show that purified Fisp12 (mCTGF) protein promotes the adhesion of microvascular endothelial cells through the integrin receptor alphavbeta3. Furthermore, Fisp12 stimulates the migration of microvascular endothelial cells in culture, also through an integrin-alphavbeta3-dependent mechanism. In addition, the presence of Fisp12 promotes endothelial cell survival when cells are plated on laminin and deprived of growth factors, a condition that otherwise induces apoptosis. In vivo, Fisp12 induces neovascularization in rat corneal micropocket implants. These results demonstrate that Fisp12 is a novel angiogenic inducer and suggest a direct role for Fisp12 in the adhesion, migration, and survival of endothelial cells during blood vessel growth. Taken together with the recent finding that the related protein CYR61 also induces angiogenesis, we suggest that Fisp12/mCTGF and CYR61 comprise prototypes of a new family of angiogenic regulators that function, at least in part, through integrin-alphavbeta3-dependent pathways. (+info)
Involvement of cis-acting repressive element(s) in the 3'-untranslated region of human connective tissue growth factor gene. (4/856)To analyze the regulatory mechanism of connective tissue growth factor expression, the 3'-untranslated region (3'-UTR) of CTGF cDNA was amplified from HeLa cell RNA. Direct nucleotide sequencing revealed a single major population in the amplicon, which was nearly identical to other sequences. Subsequently, the effect of the 3'-UTR on gene expression was evaluated. When it was fused downstream of a firefly luciferase gene, the 3'-UTR strongly repressed luciferase gene expression. Interestingly, the repressive effect of the antisense 3'-UTR appeared to be more prominent than that of the sense one. Together with the fact that several consensus sequences for regulatory elements are found in it, these results suggest the involvement of multiple sets of regulatory elements in the CTGF 3'-UTR. (+info)
Connective tissue growth factor induces the proliferation, migration, and tube formation of vascular endothelial cells in vitro, and angiogenesis in vivo. (5/856)Connective tissue growth factor (CTGF) is a novel cysteine-rich, secreted protein. Recently, we found that inhibition of the endogenous expression of CTGF by its antisense oligonucleotide and antisense RNA suppresses the proliferation and migration of vascular endothelial cells. In the present study, the following observations demonstrated the angiogenic function of CTGF in vitro and in vivo: (i) purified recombinant CTGF (rCTGF) promoted the adhesion, proliferation and migration of vascular endothelial cells in a dose-dependent manner under serum-free conditions, and these effects were inhibited by anti-CTGF antibodies; (ii) rCTGF markedly induced the tube formation of vascular endothelial cells, and this effect was stronger than that of basic fibroblast growth factor or vascular endothelial growth factor; (iii) application of rCTGF to the chicken chorioallantoic membrane resulted in a gross angiogenic response, and this effect was also inhibited by anti-CTGF antibodies. (iv) rCTGF injected with collagen gel into the backs of mice induced strong angiogenesis in vivo. These findings indicate that CTGF is a novel, potent angiogenesis factor which functions in multi-stages in this process. (+info)
Connective tissue growth factor is a regulator for fibrosis in human chronic pancreatitis. (6/856)OBJECTIVE: To evaluate the parameters that mediate fibrogenesis in chronic pancreatitis (CP). BACKGROUND: Connective tissue growth factor (CTGF), which is regulated by transforming growth factor beta (TGF-beta), has recently been implicated in skin fibrosis and atherosclerosis. In the present study, the authors analyzed the concomitant presence of TGF-beta1 and its signaling receptors-TGF-beta receptor I, subtype ALK5 (TbetaR-I(ALK5)), and TGF-beta receptor II (TbetaR-II)-as well as CTGF and collagen type I in the pancreatic tissue of patients undergoing surgery for chronic pancreatitis. PATIENTS AND METHODS: CP tissue samples were obtained from 40 patients (8 women, 32 men) undergoing pancreatic resection. Tissue samples of 25 previously healthy organ donors (12 women, 13 men) served as controls. The expression of TGF-beta1, TbetaR-I(ALK5), TbetaR-II, CTGF, and collagen type I was studied by Northern blot analysis. By in situ hybridization and immunohistochemistry, the respective mRNA moieties and proteins were localized in the tissue samples. RESULTS: Northern blot analysis showed that CP tissue samples exhibited concomitant enhanced mRNA expression of TGF-beta1 (38-fold), TbetaR-II (5-fold), CTGF (25-fold), and collagen type I (24-fold) compared with normal controls. In addition, TbetaR-I(ALK5) mRNA was increased in 50% of CP tissue samples (1.8-fold). By in situ hybridization, TGF-beta1, TbetaR-I(ALK5), and TbetaR-II mRNA were often seen to be colocalized, especially in the ductal cells and in metaplastic areas where atrophic acinar cells appeared to dedifferentiate into ductal structures. In contrast, CTGF was located in degenerating acinar cells and principally in fibroblasts surrounding these areas. Moreover, CTGF mRNA expression levels correlated positively with the degree of fibrosis in CP tissues. CONCLUSION: The concomitant overexpression of CTGF, collagen type I, TGF-beta1, and its signaling receptors in CP suggests that these proteins contribute to enhanced extracellular matrix synthesis and accumulation, resulting finally in the fibrogenesis observed in CP. (+info)
Activation-dependent adhesion of human platelets to Cyr61 and Fisp12/mouse connective tissue growth factor is mediated through integrin alpha(IIb)beta(3). (7/856)Cyr61 and connective tissue growth factor (CTGF), members of a newly identified family of extracellular matrix-associated signaling molecules, are found to mediate cell adhesion, promote cell migration and enhance growth factor-induced cell proliferation in vitro, and induce angiogenesis in vivo. We previously showed that vascular endothelial cell adhesion and migration to Cyr61 and Fisp12 (mouse CTGF) are mediated through integrin alpha(v)beta(3). Both Cyr61 and Fisp12/mCTGF are present in normal blood vessel walls, and it has been demonstrated that CTGF is overexpressed in advanced atherosclerotic lesions. In the present study, we examined whether Cyr61 and Fisp12/mCTGF could serve as substrates for platelet adhesion. Agonist (ADP, thrombin, or U46619)-stimulated but not resting platelets adhered to both Cyr61 and Fisp12/mCTGF, and this process was completely inhibited by prostaglandin I(2), which prevents platelet activation. The specificity of Cyr61- and Fisp12/mCTGF-mediated platelet adhesion was demonstrated by specific inhibition of this process with polyclonal anti-Cyr61 and anti-Fisp12/mCTGF antibodies, respectively. The adhesion of ADP-activated platelets to both proteins was divalent cation-dependent and was blocked by RGDS, HHLGGAKQAGDV, or echistatin, but not by RGES. Furthermore, this process was specifically inhibited by the monoclonal antibody AP-2 (anti-alpha(IIb)beta(3)), but not by LM609 (anti-alpha(v)beta(3)), indicating that the interaction is mediated through integrin alpha(IIb)beta(3). In a solid phase binding assay, activated alpha(IIb)beta(3), purified by RGD affinity chromatography, bound to immobilized Cyr61 and Fisp12/mCTGF in a dose-dependent and RGD-inhibitable manner. In contrast, unactivated alpha(IIb)beta(3) failed to bind to either protein. Collectively, these findings identify Cyr61 and Fisp12/mCTGF as two novel activation-dependent adhesive ligands for the integrin alpha(IIb)beta(3) on human platelets, and implicate a functional role for these proteins in hemostasis and thrombosis. (+info)
Nuclear localisation of NOVH protein: a potential role for NOV in the regulation of gene expression. (8/856)AIMS: To identify the NOV protein detected by immunofluorescence in the nucleus of human cancer cell lines to establish whether targeting to the nucleus reflects dual paracrine and intracrine biological functions of NOV, as has been reported previously for several signalling peptides and proteins. METHODS: Nuclear and cytoplasmic fractions were prepared from 143 and HeLa cells in which nuclear NOV protein was detected. Western blotting analysis of NOV proteins in both types of fractions was performed using two NOV specific antibodies. Confocal microscopy was used to visualise the nuclear NOV protein in HeLa and 143 cells. A yeast two hybrid screening system was used to isolate cDNAs encoding proteins able to interact with the human NOV protein. RESULTS: A 31/32 kDa doublet of NOV protein was identified in the nuclear fraction of 143 and HeLa cells. Because the antibodies were directed against the C-terminus of NOV, the 31/32 kDa NOV isoform is probably truncated at the N-terminus and might correspond to the secreted 32 kDa NOV isoform detected in cell culture medium. Confocal microscopy indicated that in addition to the cytoplasmic NOV protein already identified, a nuclear NOV protein was present in both the nucleoplasm and nucleoli of Hela and 143 cells. Screening of cDNA libraries prepared from HeLa cells, Epstein-Barr virus transformed lymphocytes, and normal human brain showed that the NOV protein interacts with the rpb7 subunit of RNA polymerase in a yeast two hybrid system. CONCLUSIONS: The NOV protein detected in the nucleus of 143 and HeLa cells is probably an N-terminus truncated isoform of the secreted 48 kDa NOV protein. A growing body of evidence suggests that novH expression is closely associated with differentiation in normal human tissues and that the nov gene encodes a signalling protein that belongs to an emerging family of cell growth regulators. The nuclear localisation of a NOV isoform potentially provides an additional degree of signalling specificity. The interaction of the NOV protein and the rpb7 subunit of RNA polymerase II in the two hybrid system suggests that NOV might be involved in regulating gene expression at the transcriptional level. As has already been suggested for several other nuclearly located cytokines, the NOV protein does not contain a typical nuclear localisation signal. Therefore, it is possible that it combines with either a receptor or a chaperone during its translocation. Disruption of the balance between the secreted and nuclear NOV isoforms might affect the putative autocrine and paracrine functions of NOV and might be of considerable importance in the development of cancers in which the expression of novH has been shown to be impaired. (+info)
Fibrosis can occur in response to a variety of stimuli, including inflammation, infection, injury, or chronic stress. It is a natural healing process that helps to restore tissue function and structure after damage or trauma. However, excessive fibrosis can lead to the loss of tissue function and organ dysfunction.
There are many different types of fibrosis, including:
* Cardiac fibrosis: the accumulation of scar tissue in the heart muscle or walls, leading to decreased heart function and potentially life-threatening complications.
* Pulmonary fibrosis: the accumulation of scar tissue in the lungs, leading to decreased lung function and difficulty breathing.
* Hepatic fibrosis: the accumulation of scar tissue in the liver, leading to decreased liver function and potentially life-threatening complications.
* Neurofibromatosis: a genetic disorder characterized by the growth of benign tumors (neurofibromas) made up of fibrous connective tissue.
* Desmoid tumors: rare, slow-growing tumors that are made up of fibrous connective tissue and can occur in various parts of the body.
Fibrosis can be diagnosed through a variety of methods, including:
* Biopsy: the removal of a small sample of tissue for examination under a microscope.
* Imaging tests: such as X-rays, CT scans, or MRI scans to visualize the accumulation of scar tissue.
* Blood tests: to assess liver function or detect specific proteins or enzymes that are elevated in response to fibrosis.
There is currently no cure for fibrosis, but various treatments can help manage the symptoms and slow the progression of the condition. These may include:
* Medications: such as corticosteroids, immunosuppressants, or chemotherapy to reduce inflammation and slow down the growth of scar tissue.
* Lifestyle modifications: such as quitting smoking, exercising regularly, and maintaining a healthy diet to improve overall health and reduce the progression of fibrosis.
* Surgery: in some cases, surgical removal of the affected tissue or organ may be necessary.
It is important to note that fibrosis can progress over time, leading to further scarring and potentially life-threatening complications. Regular monitoring and follow-up with a healthcare professional are crucial to managing the condition and detecting any changes or progression early on.
Some common types of connective tissue diseases include:
1. Rheumatoid arthritis (RA): A chronic autoimmune disorder that causes inflammation and joint damage.
2. Systemic lupus erythematosus (SLE): An autoimmune disorder that can affect multiple systems in the body, including the skin, joints, and kidneys.
3. Sjogren's syndrome: An autoimmune disorder that causes dry eyes and mouth, as well as joint pain and swelling.
4. Fibromyalgia: A chronic condition characterized by widespread muscle pain and fatigue.
5. Myositis: Inflammatory diseases that affect the muscles, such as dermatomyositis and polymyositis.
6. Giant cell arteritis: A condition that causes inflammation of the blood vessels, particularly in the head and neck.
7. Takayasu arteritis: A condition that causes inflammation of the blood vessels in the aorta and its branches.
8. Polyarteritis nodosa: A condition that causes inflammation of the blood vessels, particularly in the hands and feet.
9. IgG4-related disease: A condition characterized by inflammation and damage to various organs, including the pancreas, salivary glands, and liver.
Connective tissue diseases can cause a wide range of symptoms, including joint pain and stiffness, fatigue, skin rashes, fever, and weight loss. Treatment options vary depending on the specific disease and its severity, but may include medications such as nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and disease-modifying anti-rheumatic drugs (DMARDs). In some cases, surgery or physical therapy may also be necessary.
There are two main types of systemic scleroderma: diffuse cutaneous systemic sclerosis (DCSS) and limited cutaneous systemic sclerosis (LCSS). DCSS is characterized by skin thickening and scar formation over the trunk, arms, and legs, while LCSS is characterized by skin tightening and patches of scaly skin on the hands and face.
The symptoms of systemic scleroderma can include:
* Skin hardening and tightening
* Joint pain and stiffness
* Muscle weakness
* Swallowing difficulties
* Heartburn and acid reflux
* Shortness of breath
* Raynaud's phenomenon (pale or blue-colored fingers and toes in response to cold temperatures or stress)
The exact cause of systemic scleroderma is not known, but it is believed to involve a combination of genetic and environmental factors. Treatment options for systemic scleroderma include medications to manage symptoms such as pain, stiffness, and swallowing difficulties, as well as physical therapy and lifestyle modifications to improve quality of life.
In summary, systemic scleroderma is a chronic autoimmune disease that affects multiple systems in the body, causing skin hardening and thickening, fatigue, joint pain, and other symptoms. While there is no cure for systemic scleroderma, treatment options are available to manage symptoms and improve quality of life.
The exact cause of MCTD is not known, but it is believed to be an autoimmune disorder, meaning that the immune system mistakenly attacks healthy tissues in the body. The disease is more common in women than men and typically affects people between the ages of 20 and 50.
Symptoms of MCTD can vary widely and may include:
* Skin rashes or lesions
* Joint pain and stiffness
* Raynaud's phenomenon (digits turn white or blue in response to cold or stress)
* Swollen lymph nodes
* Shortness of breath
* Chest pain
* Abdominal pain
* Weakness and wasting of muscles
There is no cure for MCTD, but treatment focuses on managing symptoms and preventing complications. Medications such as nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and immunosuppressive drugs may be used to reduce inflammation and suppress the immune system. Physical therapy and exercise may also be helpful in maintaining joint mobility and strength.
The prognosis for MCTD varies depending on the severity of the disease and the presence of certain complications, such as lung or heart involvement. Some people with MCTD may experience a gradual worsening of symptoms over time, while others may experience periods of remission. With appropriate treatment, many people with MCTD are able to manage their symptoms and lead active lives.
1) They share similarities with humans: Many animal species share similar biological and physiological characteristics with humans, making them useful for studying human diseases. For example, mice and rats are often used to study diseases such as diabetes, heart disease, and cancer because they have similar metabolic and cardiovascular systems to humans.
2) They can be genetically manipulated: Animal disease models can be genetically engineered to develop specific diseases or to model human genetic disorders. This allows researchers to study the progression of the disease and test potential treatments in a controlled environment.
3) They can be used to test drugs and therapies: Before new drugs or therapies are tested in humans, they are often first tested in animal models of disease. This allows researchers to assess the safety and efficacy of the treatment before moving on to human clinical trials.
4) They can provide insights into disease mechanisms: Studying disease models in animals can provide valuable insights into the underlying mechanisms of a particular disease. This information can then be used to develop new treatments or improve existing ones.
5) Reduces the need for human testing: Using animal disease models reduces the need for human testing, which can be time-consuming, expensive, and ethically challenging. However, it is important to note that animal models are not perfect substitutes for human subjects, and results obtained from animal studies may not always translate to humans.
6) They can be used to study infectious diseases: Animal disease models can be used to study infectious diseases such as HIV, TB, and malaria. These models allow researchers to understand how the disease is transmitted, how it progresses, and how it responds to treatment.
7) They can be used to study complex diseases: Animal disease models can be used to study complex diseases such as cancer, diabetes, and heart disease. These models allow researchers to understand the underlying mechanisms of the disease and test potential treatments.
8) They are cost-effective: Animal disease models are often less expensive than human clinical trials, making them a cost-effective way to conduct research.
9) They can be used to study drug delivery: Animal disease models can be used to study drug delivery and pharmacokinetics, which is important for developing new drugs and drug delivery systems.
10) They can be used to study aging: Animal disease models can be used to study the aging process and age-related diseases such as Alzheimer's and Parkinson's. This allows researchers to understand how aging contributes to disease and develop potential treatments.
There are several types of pulmonary fibrosis, including:
1. Idiopathic pulmonary fibrosis (IPF): This is the most common and severe form of the disease, with no known cause or risk factors. It is characterized by a rapid decline in lung function and poor prognosis.
2. Connective tissue disease-associated pulmonary fibrosis: This type is associated with conditions such as rheumatoid arthritis, systemic lupus erythematosus, and scleroderma.
3. Drug-induced pulmonary fibrosis: Certain medications, such as amiodarone and nitrofurantoin, can cause lung damage and scarring.
4. Radiation-induced pulmonary fibrosis: Exposure to high doses of radiation, especially in childhood, can increase the risk of developing pulmonary fibrosis later in life.
5. Environmental exposures: Exposure to pollutants such as silica, asbestos, and coal dust can increase the risk of developing pulmonary fibrosis.
Symptoms of pulmonary fibrosis include shortness of breath, coughing, and fatigue. The disease can be diagnosed through a combination of imaging tests such as chest X-rays, computed tomography (CT) scans, and magnetic resonance imaging (MRI), as well as lung biopsy.
Treatment options for pulmonary fibrosis are limited and vary depending on the underlying cause of the disease. Medications such as pirfenidone and nintedanib can help slow the progression of the disease, while lung transplantation may be an option for advanced cases.
There are several types of diabetic nephropathy, including:
1. Mesangial proliferative glomerulonephritis: This is the most common type of diabetic nephropathy and is characterized by an overgrowth of cells in the mesangium, a part of the glomerulus (the blood-filtering unit of the kidney).
2. Segmental sclerosis: This type of diabetic nephropathy involves the hardening of some parts of the glomeruli, leading to decreased kidney function.
3. Fibrotic glomerulopathy: This is a rare form of diabetic nephropathy that is characterized by the accumulation of fibrotic tissue in the glomeruli.
4. Membranous nephropathy: This type of diabetic nephropathy involves the deposition of immune complexes (antigen-antibody complexes) in the glomeruli, leading to inflammation and damage to the kidneys.
5. Minimal change disease: This is a rare form of diabetic nephropathy that is characterized by minimal changes in the glomeruli, but with significant loss of kidney function.
The symptoms of diabetic nephropathy can be non-specific and may include proteinuria (excess protein in the urine), hematuria (blood in the urine), and decreased kidney function. Diagnosis is typically made through a combination of physical examination, medical history, laboratory tests, and imaging studies such as ultrasound or CT scans.
Treatment for diabetic nephropathy typically involves managing blood sugar levels through lifestyle changes (such as diet and exercise) and medication, as well as controlling high blood pressure and other underlying conditions. In severe cases, dialysis or kidney transplantation may be necessary. Early detection and management of diabetic nephropathy can help slow the progression of the disease and improve outcomes for patients with this condition.
Types of Experimental Diabetes Mellitus include:
1. Streptozotocin-induced diabetes: This type of EDM is caused by administration of streptozotocin, a chemical that damages the insulin-producing beta cells in the pancreas, leading to high blood sugar levels.
2. Alloxan-induced diabetes: This type of EDM is caused by administration of alloxan, a chemical that also damages the insulin-producing beta cells in the pancreas.
3. Pancreatectomy-induced diabetes: In this type of EDM, the pancreas is surgically removed or damaged, leading to loss of insulin production and high blood sugar levels.
Experimental Diabetes Mellitus has several applications in research, including:
1. Testing new drugs and therapies for diabetes treatment: EDM allows researchers to evaluate the effectiveness of new treatments on blood sugar control and other physiological processes.
2. Studying the pathophysiology of diabetes: By inducing EDM in animals, researchers can study the progression of diabetes and its effects on various organs and tissues.
3. Investigating the role of genetics in diabetes: Researchers can use EDM to study the effects of genetic mutations on diabetes development and progression.
4. Evaluating the efficacy of new diagnostic techniques: EDM allows researchers to test new methods for diagnosing diabetes and monitoring blood sugar levels.
5. Investigating the complications of diabetes: By inducing EDM in animals, researchers can study the development of complications such as retinopathy, nephropathy, and cardiovascular disease.
In conclusion, Experimental Diabetes Mellitus is a valuable tool for researchers studying diabetes and its complications. The technique allows for precise control over blood sugar levels and has numerous applications in testing new treatments, studying the pathophysiology of diabetes, investigating the role of genetics, evaluating new diagnostic techniques, and investigating complications.
FEH is considered a precancerous condition, as it has the potential to progress to cervical or endometrial cancer if left untreated. However, with early detection and appropriate treatment, the risk of progression to cancer is low.
The symptoms of FEH are not specific and can include vaginal bleeding, abnormal discharge, pain during sex, and pelvic pain. The condition is typically diagnosed through a pap smear or colposcopy, which can identify abnormal cells in the cervix or endometrium.
Treatment for FEH usually involves removal of the affected tissue through a procedure called loop electrosurgical excision procedure (LEEP) or cold knife cone biopsy. In some cases, hysterectomy may be recommended if the condition is severe or persistent.
It is important for women to practice good gynecologic health, including regular pap smears and pelvic exams, to detect any abnormalities early on and prevent the progression of FEH to cancer.
Gingival fibromatosis is relatively rare and usually does not require treatment unless it becomes inflamed or infected. Treatment options may include antibiotics, surgical removal of the growth, or other methods to reduce inflammation and improve oral hygiene.
* Gingival fibroma
* Pyogenic granuloma
* Peripheral giant cell granuloma
* Fibromatous hyperplasia of the gingiva
Note: The term "fibromatosis" refers to the excessive growth of fibrous tissue, which can occur in various parts of the body. In the context of oral health, it specifically refers to the growth of fibrous tissue on the gums.
A type of inflammatory kidney disease that affects the interstitial tissue surrounding the tubules of the kidney. It is characterized by inflammation and fibrosis (scarring) of the interstitium, leading to impaired kidney function. The exact cause of interstitial nephritis is not always known, but it can be triggered by a variety of factors, including infections, allergic reactions, and certain medications. Symptoms may include fever, joint pain, and loss of appetite, and the condition can progress to end-stage renal disease if left untreated. Treatment typically involves medication to reduce inflammation and manage symptoms, as well as supportive care to help the kidneys function properly.
Pathologic neovascularization can be seen in a variety of conditions, including cancer, diabetic retinopathy, and age-related macular degeneration. In cancer, for example, the formation of new blood vessels can help the tumor grow and spread to other parts of the body. In diabetic retinopathy, the growth of new blood vessels in the retina can cause vision loss and other complications.
There are several different types of pathologic neovascularization, including:
* Angiosarcoma: a type of cancer that arises from the cells lining blood vessels
* Hemangiomas: benign tumors that are composed of blood vessels
* Cavernous malformations: abnormal collections of blood vessels in the brain or other parts of the body
* Pyogenic granulomas: inflammatory lesions that can form in response to trauma or infection.
The diagnosis of pathologic neovascularization is typically made through a combination of physical examination, imaging studies (such as ultrasound, CT scans, or MRI), and biopsy. Treatment options vary depending on the underlying cause of the condition, but may include medications, surgery, or radiation therapy.
In summary, pathologic neovascularization is a process that occurs in response to injury or disease, and it can lead to serious complications. It is important for healthcare professionals to be aware of this condition and its various forms in order to provide appropriate diagnosis and treatment.
Treatment for ureteral obstruction depends on the underlying cause and may include medications, endoscopic procedures, or surgery. In some cases, a temporary drainage catheter may be placed in the ureter to help relieve symptoms until the blockage can be fully treated.
Ureteral obstruction can be acute or chronic, and may occur in adults or children. It is important to seek medical attention if symptoms persist or worsen over time, as untreated ureteral obstruction can lead to complications such as kidney damage or sepsis.
Causes of Ureteral Obstruction:
Ureteral obstruction can be caused by a variety of factors, including:
1. Kidney stones: Small, hard mineral deposits that form in the urine and can block the flow of urine through the ureters.
2. Tumors: Cancerous or non-cancerous growths that can block the ureters.
3. Scar tissue: Scarring from previous surgeries or injuries can cause narrowing or blockages in the ureters.
4. Prostate enlargement: In men, an enlarged prostate gland can press on the urethra and ureters, causing blockages.
5. Bladder neck obstruction: A condition where the bladder neck is narrow or blocked, preventing urine from flowing through the urethra.
6. Trauma: Injuries to the ureters or bladder can cause blockages.
7. Inflammation: Inflammation in the ureters or kidneys can cause swelling and blockages.
8. Congenital conditions: Some people may be born with abnormalities that cause blockages in the urinary tract.
9. Neurological disorders: Conditions such as multiple sclerosis, Parkinson's disease, or spinal cord injuries can affect the nerves that control the bladder and ureters, leading to blockages.
10. Medications: Certain medications, such as certain antibiotics and chemotherapy drugs, can cause damage to the ureters and lead to blockages.
Types of Kidney Diseases:
1. Acute Kidney Injury (AKI): A sudden and reversible loss of kidney function that can be caused by a variety of factors, such as injury, infection, or medication.
2. Chronic Kidney Disease (CKD): A gradual and irreversible loss of kidney function that can lead to end-stage renal disease (ESRD).
3. End-Stage Renal Disease (ESRD): A severe and irreversible form of CKD that requires dialysis or a kidney transplant.
4. Glomerulonephritis: An inflammation of the glomeruli, the tiny blood vessels in the kidneys that filter waste products.
5. Interstitial Nephritis: An inflammation of the tissue between the tubules and blood vessels in the kidneys.
6. Kidney Stone Disease: A condition where small, hard mineral deposits form in the kidneys and can cause pain, bleeding, and other complications.
7. Pyelonephritis: An infection of the kidneys that can cause inflammation, damage to the tissues, and scarring.
8. Renal Cell Carcinoma: A type of cancer that originates in the cells of the kidney.
9. Hemolytic Uremic Syndrome (HUS): A condition where the immune system attacks the platelets and red blood cells, leading to anemia, low platelet count, and damage to the kidneys.
Symptoms of Kidney Diseases:
1. Blood in urine or hematuria
2. Proteinuria (excess protein in urine)
3. Reduced kidney function or renal insufficiency
4. Swelling in the legs, ankles, and feet (edema)
5. Fatigue and weakness
6. Nausea and vomiting
7. Abdominal pain
8. Frequent urination or polyuria
9. Increased thirst and drinking (polydipsia)
10. Weight loss
Diagnosis of Kidney Diseases:
1. Physical examination
2. Medical history
3. Urinalysis (test of urine)
4. Blood tests (e.g., creatinine, urea, electrolytes)
5. Imaging studies (e.g., X-rays, CT scans, ultrasound)
6. Kidney biopsy
7. Other specialized tests (e.g., 24-hour urinary protein collection, kidney function tests)
Treatment of Kidney Diseases:
1. Medications (e.g., diuretics, blood pressure medication, antibiotics)
2. Diet and lifestyle changes (e.g., low salt intake, increased water intake, physical activity)
3. Dialysis (filtering waste products from the blood when the kidneys are not functioning properly)
4. Kidney transplantation ( replacing a diseased kidney with a healthy one)
5. Other specialized treatments (e.g., plasmapheresis, hemodialysis)
Prevention of Kidney Diseases:
1. Maintaining a healthy diet and lifestyle
2. Monitoring blood pressure and blood sugar levels
3. Avoiding harmful substances (e.g., tobacco, excessive alcohol consumption)
4. Managing underlying medical conditions (e.g., diabetes, high blood pressure)
5. Getting regular check-ups and screenings
Early detection and treatment of kidney diseases can help prevent or slow the progression of the disease, reducing the risk of complications and improving quality of life. It is important to be aware of the signs and symptoms of kidney diseases and seek medical attention if they are present.
The condition can be caused by a variety of factors, including excessive alcohol consumption, viral hepatitis, non-alcoholic fatty liver disease, and certain medications. It can also be a complication of other diseases such as hemochromatosis and Wilson's disease.
The symptoms of liver cirrhosis can vary depending on the severity of the disease, but may include fatigue, loss of appetite, nausea, abdominal swelling, and pain in the upper right side of the abdomen. As the disease progresses, it can lead to complications such as esophageal varices, ascites, and liver failure, which can be life-threatening.
There is no cure for liver cirrhosis, but treatment options are available to manage the symptoms and slow the progression of the disease. These may include medications to control swelling and pain, dietary changes, and in severe cases, liver transplantation. In some cases, a liver transplant may be necessary if the disease has caused significant damage and there is no other option to save the patient's life.
In conclusion, liver cirrhosis is a serious and potentially life-threatening condition that can cause significant damage to the liver and lead to complications such as liver failure. It is important for individuals to be aware of the risk factors and symptoms of the disease in order to seek medical attention if they suspect they may have liver cirrhosis. With proper treatment and management, it is possible to slow the progression of the disease and improve the patient's quality of life.
WNT1-inducible-signaling pathway protein 1
Vascular endothelial growth factor A
Mir-504 microRNA precursor family
Mir-346 microRNA precursor family
Bone growth factor
Mothers against decapentaplegic homolog 3
Transforming growth factor, beta 3
Mir-30 microRNA precursor
TGF beta 2
Insulin-like growth factor 2 receptor
Pancreatic stellate cell
Von Willebrand factor type C domain
CKLF-like MARVEL transmembrane domain-containing 5
Physiological effects in space
Low-grade myofibroblastic sarcoma
Innate immune system
Matthew H. Liang
Platelet-derived growth factor
List of skin conditions
White blood cell
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- Connective tissue growth factor (CTGF) has been shown to be substantially involved in various processes of fibrosis. (nih.gov)
- Connective tissue growth factor (CTGF) has been previously implicated in cancer metastasis and invasion in various tumors. (nih.gov)
- Quantitative RT-PCR was used to asses mRNA levels of collagenase-1 (MMP-1), stromelysin (MMP-3), vascular endothelial growth factor (VEGF), connective tissue growth factor (CTGF), cyclooxygenase-2 (COX-2), interleukin-1β (IL-1β), type III collagen (COL-III) and fibronectin (FBRN). (cdc.gov)
- 15. Connective-tissue growth factor (CTGF) modulates cell signalling by BMP and TGF-beta. (nih.gov)
- Expression of mRNA for tumor necrosis factor-alpha (TNF-alpha), interleukin-10 (IL-10), matrix metalloproteinase-9, and connective tissue growth factor (CTGF) also increased in the liver following acetaminophen treatment of wild-type mice. (nih.gov)
- Connective tissue growth factor (CTGF) is a key negative regulator of adipocytic differentiation of BMSCs ( 20 ). (frontiersin.org)
- 23. Requirement for active glycogen synthase kinase-3β in TGF-β1 upregulation of connective tissue growth factor (CCN2/CTGF) levels in human gingival fibroblasts. (nih.gov)
- CCN2, formerly known as CTGF, a major connective tissue mitoattractant secreted by vascular endothelial cells, promotes proliferation and differentiation of chondrocytes. (nih.gov)
- The unique unbiased screening approach employed by AivoCode to probe the vasculature in AD has identified a novel target, connective tissue growth factor (CTGF), which is involved in vascular dysfunction and neuroinflammation. (nih.gov)
- A number of papers have suggested that caffeine, and in particular its main primary metabolite, paraxanthine, can suppress the synthesis of CTGF (connective tissue growth factor) via a cascade of control cycles, thereby slowing down the growth of this type of tissue, which in turn slows down the progression of liver fibrosis, alcoholic cirrhosis and liver cancer 10,26,30,48 . (coffeeandhealth.org)
- Fibrosis can be caused by profibrotic cytokines, including transforming growth factor-beta (TGF-beta), interleukin-4 (IL-4), platelet-derived growth factor (PDGF), and connective-tissue growth factor. (medscape.com)
- Multiple pathways have been found to trigger EMT: tyrosine kinase receptors (epidermal growth factor, fibroblast growth factor, connective tissue growth factor, platelet-derived growth factor, insulin-like growth factor, etc), integrins, Wnt, nuclear factor (NF)-κB and transforming growth factor β (TGF-β) pathways. (bmj.com)
- 40. The context-dependent role of transforming growth factor-β/miR-378a-3p/connective tissue growth factor in vascular calcification: a translational study. (nih.gov)
- 7. [Expression of cysteine rich 61 and vascular endothelial growth factor genes in patients with myelodysplastic syndromes and their relationship. (nih.gov)
- 12. [Dynamic observation of vascular endothelial growth factor (VEGF)/VEGF-receptors expression in acute leukemia]. (nih.gov)
- 15. Expression of vascular endothelial growth factor-C and its receptor in osteosarcomas. (nih.gov)
- 17. Overexpression of vascular endothelial growth factor (VEGF) and its cellular receptor KDR (VEGFR-2) in the bone marrow of patients with acute myeloid leukemia. (nih.gov)
- Many factors, including environmental factors, can lead to immunologic system disturbances and vascular changes. (medscape.com)
- Activation of the nuclear receptor peroxisome proliferator-activated receptor gamma (PPAR-γ) and fibroblast growth factor 21 (FGF21) promotes adipocyte differentiation but is also known to inhibit osteoblast differentiation ( 21 , 22 ). (frontiersin.org)
- It enhances fibroblast growth factor-induced DNA synthesis. (nih.gov)
- Dysregulated actions of bone-derived phosphaturic hormone fibroblast growth factor 23 (FGF23) result in several inherited diseases, such as X-linked hypophosphatemia (XLH), and contribute substantially to the mortality in kidney failure. (jci.org)
- In addition to cells resembling those of the uterine wall, fibroid tumors are made up of extracellular matrix, the fibrous connective meshwork that holds cells in place. (nih.gov)
- EGCG treatment significantly lowered the levels of fibronectin, a key extracellular matrix protein and connective tissue growth factor protein. (nih.gov)
- 1. The connective tissue growth factor/cysteine-rich 61/nephroblastoma overexpressed (CCN) family. (nih.gov)
- 2. Expression of the Elm1 gene, a novel gene of the CCN (connective tissue growth factor, Cyr61/Cef10, and neuroblastoma overexpressed gene) family, suppresses In vivo tumor growth and metastasis of K-1735 murine melanoma cells. (nih.gov)
- More recent work has revealed that BMF plays an important role in energy storage, endocrine function, bone metabolism, and regulation of the growth and metastasis of tumors ( 2 , 5 - 7 ). (frontiersin.org)
- 30. Connective tissue growth factor inhibits metastasis and acts as an independent prognostic marker in colorectal cancer. (nih.gov)
- Pseudoaneurysm denotes a ruptured aortic wall with healing of the extravasated blood and formation of the aneurysm wall by fibrous tissue. (medscape.com)
- growth suppression (a) paralled the increased fibroblast PGE synthesis, (b) was reversed by addition of inhibitors of prostaglandin synthesis (indomethacin, meclofenamate, and eicostaetraynoic acid), and (c) was reproduced by addition of exogenous PGE2 to fibroblast cultures. (jci.org)
- While this growth factor by itself is unlikely to produce significant spinal cord regeneration in human patients, the findings do offer a promising lead for researchers pursuing the next generation of regenerative therapies. (nih.gov)
- Additionally, recent research has demonstrated that stem cell treatment can be used as a treatment approach for wound repair and tissue regeneration, such as adipose-derived stem cells (ADSCs) and bone marrow-derived stem cells, which have been studied under both pre-clinical and clinical conditions ( 11 ). (spandidos-publications.com)
- The fat in the bone marrow is different from the subcutaneous and visceral fat and exists in two distinct populations: constitutive marrow adipose tissue (cMAT) and regulated marrow adipose tissue (rMAT). (frontiersin.org)
- 5. Expressions of cysteine-rich61, connective tissue growth factor and Nov genes in hepatocellular carcinoma and their clinical significance. (nih.gov)
- A common feature of these pathways is that they activate 'master transcription factors' (Snail, Slug, Zeb-1, Twist, etc) which switch on the EMT programme in epithelial cells, namely, downregulating E-cadherin expression and other genes linked to the epithelial phenotype and activating the transcription of genes associated with the mesenchymal phenotype. (bmj.com)
- They've discovered that the zebrafish's damaged cells secrete a molecule known as connective tissue growth factor a (CTGFa) that is essential in regenerating its severed spinal cord. (nih.gov)
- Different regulatory mechanisms between mRNA and protein expression or localized changes missed due to homogenization of the tissue samples, may explain the discrepancy in findings. (cdc.gov)
- 6. Nephroblastoma overexpressed gene (NOV) codes for a growth factor that induces protein tyrosine phosphorylation. (nih.gov)
- 7. CCN proteins are distinct from, and should not be considered members of, the insulin-like growth factor-binding protein superfamily. (nih.gov)
- Increased collagen deposition in tissues is a characteristic feature of systemic sclerosis. (medscape.com)
- Increased collagen production or disturbances in its degradation can cause excessive collagen deposition in tissues. (medscape.com)
- Wound healing is an extremely dynamic process that includes a variety of cellular and biochemical processes, of which dermis collagen remodeling and scar budding are two important parts of tissue repair during the maturation phase ( 3 ). (spandidos-publications.com)
- Fibroblasts are a type of mesenchymal cell in connective tissue and have a significant role in depositing the collagen and elastic fibers of the ECM ( 10 ). (spandidos-publications.com)
- Scars, which are harmful to normal tissue function, are created during skin wound healing and are specifically caused by excessive deposition of the ECM by fibroblasts and myofibroblasts ( 5 ). (spandidos-publications.com)
- It has been demonstrated that the heterogeneity of fibroblasts exerts positive effects on wound healing without scar formation and full recovery of the native tissue structures in fetuses and the oral mucosa ( 8 ). (spandidos-publications.com)
- Understanding these processes is crucial for elucidating pathomechanisms of connective tissue disorders characterized by ECM deficiency and growth factor dysregulation. (jbc.org)
- EMT is thought to be involved in the pathogenesis of numerous lung diseases ranging from developmental disorders, fibrotic tissue remodelling to lung cancer. (bmj.com)
- Patients with idiopathic, noninflammatory aneurysms are typically adults and present with symptoms of aneurysm later than do those individuals with identified connective tissue disorders. (medscape.com)
- When the fish's spinal cord is severed, something remarkable happens that doesn't occur in humans: supportive cells in the nervous system bridge the gap, allowing new nerve tissue to restore the spinal cord to full function within weeks. (nih.gov)
- Bone marrow adipocytes (BMAs), as a component of the bone marrow microenvironment, influence hematopoiesis through direct contact with cells and the secretion of adipocyte-derived factors. (frontiersin.org)
- Epigallocatechin gallate (EGCG), a compound found in green tea, appears to inhibit the biochemical processes that promote the growth and development of fibroid tumors cells, suggests a study funded in part by the National Institutes of Health. (nih.gov)
- Previous studies have shown that EGCG inhibited the growth of human uterine fibroid cells in laboratory cultures. (nih.gov)
- For the current study, the authors treated cultures of patients' fibroid cells with EGCG to gain insights into how EGCG might affect the biochemical processes underlying the growth of fibroid cells. (nih.gov)
- Similarly, EGCG disrupted biochemical pathways involved in fibroid cell growth, movement, metabolism, and signaling-the process cells use to send chemical messages that trigger their growth, development, and other activities. (nih.gov)
- Partially via defined oligopeptide sequences or structural domains, the ECM transfers specific signals to cells that act in concert with growth factors/cytokines. (thieme-connect.com)
- Connective tissue growth factor expression in the rat remnant kidney model and association with tubular epithelial cells undergoing transdifferentiation. (nih.gov)
- Activation of canonical Wnt signalling and β catenin makes epithelial cells susceptible to EMT caused by TGF-β, by inhibiting the growth arrest which is induced by TGF-β. (bmj.com)
- The prostaglandin-stimulatory, growth-suppressive activity was a product of non-T-lymphocyte, adherent cells and was present within 6 h of mononuclear cell culture. (jci.org)
- 27. Connective tissue growth factor gene expression alters tumor progression in esophageal cancer. (nih.gov)
- It consists of collagens, glycoproteins, proteoglycans, glycosaminoglycans and molecules that are bound specifically by the ECM, such as certain growth factors/cytokines, matrix metalloproteinases (MMPs) and processing enzymes such as tissue transglutaminase and procollagen propeptidases. (thieme-connect.com)
- Caffeine not only represses the activation of these myofibroblasts, but also expression of a connective tissue growth factor. (medscape.com)
- 21. [Expression of connective tissue growth factor in colorectal cancer and its association with prognosis]. (nih.gov)
- 25. Differential expression of transforming growth factor-beta1, connective tissue growth factor, phosphorylated-SMAD2/3 and phosphorylated-ERK1/2 during mouse tooth development. (nih.gov)
- 26. Activation of TGF-beta within cultured hepatocytes and in liver injury leads to intracrine signaling with expression of connective tissue growth factor. (nih.gov)
- 39. Kinetics of connective tissue growth factor expression during experimental proliferative glomerulonephritis. (nih.gov)
- In the present studies, we used transgenic mice with a targeted disruption of the gene for inducible nitric oxide synthase (NOS II) to analyze the role of nitric oxide in inflammatory mediator production in the liver and in tissue injury induced by acetaminophen. (nih.gov)
- In advanced stages, however, systemic intervention is required to inhibit tumor growth and prevent secondary metastases. (oncotarget.com)
- The role of immune cell products in modulating connective tissue metabolism was investigated. (jci.org)
- Microfibrils become part of the fibers that provide strength and flexibility to connective tissue that supports the body's joints and organs. (medlineplus.gov)
- The term "oncotarget" encompasses all molecules, pathways, cellular functions, cell types, and even tissues that can be viewed as targets relevant to cancer as well as other diseases. (oncotarget.com)
- 28. Role of transforming growth factor-beta signaling pathway in pathogenesis of benign biliary stricture. (nih.gov)
- Several transcription factors such as Snail, Slug, ZEB-1, ZEB-2, Twist, β-catenin and Tcf/LEF have been identified as key regulators of EMT, and are the 'master switches' important for cell reprogramming ( figure 1 ). (bmj.com)
- 3. Elevated levels of connective tissue growth factor, WISP-1, and CYR61 in primary breast cancers associated with more advanced features. (nih.gov)
- Reduced hepatotoxicity of acetaminophen in mice lacking inducible nitric oxide synthase: potential role of tumor necrosis factor-alpha and interleukin-10. (nih.gov)
- 31. [The role of connective tissue growth factor, transforming growth factor and Smad signaling pathway during corneal wound healing]. (nih.gov)
- Wound healing is a complex process in which tissue homeostasis and the protective role of the skin are restored ( 1 ). (spandidos-publications.com)
- Systemic sclerosis (SSc) is a systemic connective tissue disease. (medscape.com)
- 22. Immunolocalization of connective tissue growth factor, transforming growth factor-beta1 and phosphorylated-SMAD2/3 during the postnatal tooth development and formation of junctional epithelium. (nih.gov)
- A number of factors are postulated to increase the risk of the development of PPCM. (internationaljournalofcardiology.com)
- 36. MicroRNA‑133b inhibits connective tissue growth factor in colorectal cancer and correlates with the clinical stage of the disease. (nih.gov)
- The increasing prevalence of AD and mild cognitive impairment across the aging population, together with advances in diagnostic capability and increased social awareness of the disease, will contribute further to market growth. (nih.gov)
- Growth factors enable the growth and repair of tissues throughout the body. (medlineplus.gov)
- We searched MEDLINE (January 1966-September 2007), OVID, and reference lists of articles for studies containing information on the aetiology and risk factors for PPCM, and published in English. (internationaljournalofcardiology.com)
- Additionally, microfibrils regulate the activity of molecules called growth factors. (medlineplus.gov)
- In addition, single-domain antibodies offer advantages over conventional monoclonal antibodies, including smaller size, improved stability, and better penetration through tissue and barriers, including the blood-brain barrier. (nih.gov)
- In a study of 82 consecutive unoperated patients with TAA who underwent serial aneurysm measurements, Cheung et al found that TAA growth rates were greater in women than in men, and that this difference was specific to women with degenerative TAAs. (medscape.com)
- Examples are peptides derived from collagens VI (stress activation) and XIV (stress relaxation), or collagenous consensus peptides that remove ECM-bound MMPs and growth factors. (thieme-connect.com)
- Together with a third related gene, WISP-3, these proteins define a subfamily of the connective tissue growth factor family. (nih.gov)
- The literature reveals a wealth of articles proposing various mechanisms for aetiology and risk factors of PPCM. (internationaljournalofcardiology.com)
- This study analyzed the efficacy and safety of ARNI in the treatment of heart failure, and analyzed the risk factors for readmission after ARNI treatment. (bvsalud.org)
- The aetiology and risk factors for PPCM are poorly defined. (internationaljournalofcardiology.com)