AnatomyOrganismsDiseasesChemicals and DrugsAnalytical, Diagnostic and Therapeutic Techniques and EquipmentPhenomena and ProcessesDisciplines and OccupationsInformation ScienceHealth Care
FibrosisCystic FibrosisConnective Tissue Growth FactorCystic Fibrosis Transmembrane Conductance RegulatorEndomyocardial FibrosisIdiopathic Pulmonary FibrosisImmediate-Early ProteinsLiver CirrhosisIntercellular Signaling Peptides and ProteinsRetroperitoneal FibrosisTransforming Growth Factor betaBleomycinFibroblastsLungOral Submucous FibrosisCollagen Type ILiver Cirrhosis, ExperimentalCollagenHepatic Stellate CellsDisease Models, AnimalUreteral ObstructionHydroxyprolinePeritoneal FibrosisMyofibroblastsCollagen Type IIIPseudomonas InfectionsRNA, MessengerCells, CulturedCarbon TetrachlorideScleroderma, SystemicCysteine-Rich Protein 61Transforming Growth Factor beta1Pseudomonas aeruginosaMice, Inbred C57BLBiopsyExtracellular MatrixLiverGrowth SubstancesSignal TransductionKidneySmad3 ProteinGene Expression RegulationNephritis, InterstitialSweatSputumEpithelial CellsSmad2 ProteinSmad ProteinsReverse Transcriptase Polymerase Chain ReactionActinsMyocardiumDisease ProgressionKidney TubulesImmunohistochemistryMice, KnockoutGene ExpressionMice, Inbred CFTRFibronectinsRats, Sprague-DawleyLiver Diseases, ParasiticBiological MarkersHepatitis C, ChronicKidney DiseasesTime FactorsBurkholderia InfectionsBurkholderia cepaciaBlotting, WesternNephrogenic Fibrosing DermopathyUp-RegulationCell LineElasticity Imaging TechniquesChloridesInflammationFatty LiverRespiratory MucosaBronchoalveolar Lavage FluidRespiratory Function TestsMesangial CellsMice, TransgenicTissue Inhibitor of Metalloproteinase-1Cell ProliferationLung DiseasesRats, WistarExtracellular Matrix ProteinsLung Diseases, InterstitialBronchiectasisReceptors, Transforming Growth Factor betaPhenotypeSeverity of Illness IndexExocrine Pancreatic InsufficiencyCardiomegalyTransforming Growth Factor beta2Chronic DiseaseSkinVentricular RemodelingMutationGlomerular MesangiumSmad7 ProteinAlanine TransaminaseThioacetamide
ConnectivePulmonaryInflammationPamrevlumabCystic fibrosisLiver fibrosisCardiac fibrosisCollagenMonoclonal AntibodyFibroticRenalPathwaysPathologicPromotesDysfunctionMechanismsMechanismProgressive fibrosisProteinExpressionMyocardial infarctionPathologicalHypoxiaVitroVascularTissue RepairManifestationInhibitionBiomarkerEffectorPathogenesisWoundSignificantlyCellularInhibitDiseases
Connective12
Pulmonary36
  • Pulmonary fibrosis is a condition in which the lungs become scarred over time. (wikipedia.org)
  • However, in most cases the cause is unknown, and termed idiopathic pulmonary fibrosis. (wikipedia.org)
  • Lung sound in idiopathic pulmonary fibrosis velcro crackles on auscultation in a person with idiopathic pulmonary fibrosis Problems playing this file? (wikipedia.org)
  • Symptoms of pulmonary fibrosis are mainly: Shortness of breath, particularly with exertion Chronic dry, hacking coughing Fatigue and weakness Chest discomfort including chest pain Loss of appetite and rapid weight loss Pulmonary fibrosis is suggested by a history of progressive shortness of breath (dyspnea) with exertion. (wikipedia.org)
  • Pulmonary fibrosis may be a secondary effect of other diseases. (wikipedia.org)
  • However, pulmonary fibrosis can also appear without any known cause. (wikipedia.org)
  • Most idiopathic cases are diagnosed as idiopathic pulmonary fibrosis. (wikipedia.org)
  • For example, a mutation in surfactant protein C (SP-C) has been found to exist in some families with a history of pulmonary fibrosis. (wikipedia.org)
  • Autosomal dominant mutations in the TERC or TERT genes, which encode telomerase, have been identified in about 15 percent of pulmonary fibrosis patients. (wikipedia.org)
  • Diseases and conditions that may cause pulmonary fibrosis as a secondary effect include: Inhalation of environmental and occupational pollutants, such as metals in asbestosis, silicosis and exposure to certain gases. (wikipedia.org)
  • Such scar tissue causes an irreversible decrease in oxygen diffusion capacity, and the resulting stiffness or decreased compliance makes pulmonary fibrosis a restrictive lung disease. (wikipedia.org)
  • Pulmonary fibrosis is perpetuated by aberrant wound healing, rather than chronic inflammation. (wikipedia.org)
  • In contrast, quadriplegia and kyphosis are examples of causes of restrictive lung disease that do not necessarily involve pulmonary fibrosis. (wikipedia.org)
  • Idiopathic pulmonary fibrosis: multiple causes and multiple mechanisms? (ersjournals.com)
  • Idiopathic pulmonary fibrosis (IPF) is a devastating condition that carries a prognosis worse than that of many cancers. (ersjournals.com)
  • It is argued here, instead, that abnormalities in multiple pathways involved in wound healing and inflammation lead to the development of idiopathic pulmonary fibrosis, and it is suggested that a new rationale for clinical classification and pathogenesis may be more productive in driving the search for novel therapies in the future. (ersjournals.com)
  • Idiopathic pulmonary fibrosis (IPF) is a devastating, progressive fibrotic lung condition that carries a median survival of 2.8-4.2 yrs, and for which no effective treatments exist 1 , 2 . (ersjournals.com)
  • The clinical manifestations are renal disease, idiopathic pulmonary fibrosis (IPF), heart failure, end-stage liver diseases, and so on ( Bataller and Brenner, 2005 ). (frontiersin.org)
  • The therapeutic effect of umbilical cord-derived mesenchymal stem cells(hUC-MSCs) in combination with pirfenidone(PFD) on pulmonary fibrosis in mice and its possible mechanism were investigated. (researchsquare.com)
  • Pulmonary myofibroblasts were divided into MFB group and MFB + hUC-MSCs group, and different doses of PFD were added to each group, and the levels of RGS2 and fibrosis markers were detected in each group. (researchsquare.com)
  • Its effect attenuating bleomycin-induced pulmonary fibrosis in mice is related with the increase of RGS2. (researchsquare.com)
  • Idiopathic pulmonary fibrosis (IPF) represents probably the most aggressive form of ILD and systemic sclerosis is a multiorgan fibrotic disease frequently associated with ILD. (ersjournals.com)
  • Some forms of fibrosis, such as acute lung injury or cryptogenic organising pneumonia, are at least partially reversible, whereas others, in particular idiopathic pulmonary fibrosis (IPF), are progressive and fatal. (ersjournals.com)
  • In systemic sclerosis (SSc) patients, the change in the trend of scleroderma-related deaths over the past 30 years demonstrates that lung involvement (both pulmonary hypertension and pulmonary fibrosis) is among the primary causes of mortality [ 6 ]. (ersjournals.com)
  • In SSc, pulmonary disease can exist as a heterogeneous combination of pulmonary fibrosis and pulmonary arterial hypertension (PAH), but the pathogenic mechanisms that induce different pulmonary responses are poorly understood. (ersjournals.com)
  • This schematic view of the morpho-functional unit of the lung (alveolus) depicts the main differences in cellular composition in idiopathic pulmonary fibrosis (IPF) and systemic sclerosis-associated interstitial lung disease (SSc-ILD) compared with normal physiological cellular components. (ersjournals.com)
  • The poster also includes preclinical data demonstrating a favorable profile of PRS-220 for inhaled delivery and CTGF targeting in the lung, including a superior lung biodistribution profile compared to a systemically administered anti-CTGF monoclonal antibody, a lung PK profile supporting once or twice daily dosing in humans, and desired aerosol performance upon nebulization to effectively target pulmonary tissue of interest. (bignewsnetwork.com)
  • Based on the pulmonary pathophysiology associated with IPF, we believe that directly inhibiting CTGF in the lung with an inhaled therapy could result in more efficient target saturation, superior clinical efficacy, and greater convenience for patients,' said Shane Olwill Ph.D., Chief Development Officer at Pieris. (bignewsnetwork.com)
  • STAT4 is a genetic risk factor for systemic sclerosis having additive effects with IRF5 on disease susceptibility and related pulmonary fibrosis. (cdc.gov)
  • Association between the IRF5 rs2004640 functional polymorphism and systemic sclerosis: a new perspective for pulmonary fibrosis. (cdc.gov)
  • The status of pulmonary fibrosis in systemic sclerosis is associated with IRF5, STAT4, IRAK1, and CTGF polymorphisms. (cdc.gov)
  • Lung tissues of patients with RIPF and idiopathic pulmonary fibrosis, and lung tissues from various fibrotic mouse models, as well as appropriated cell line systems were used. (biomedcentral.com)
  • Pulmonary fibrosis (PF) is a chronic and fatal interstitial lung disease involving deposition of collagen and extracellular matrix (ECM) around the fibrotic foci, as well as honeycomb changes of the subpleural and basement membranes. (biomedcentral.com)
  • The most common type of PF is idiopathic pulmonary fibrosis (IPF), with a median survival of only 2-4 years [ 1 ]. (biomedcentral.com)
  • A Phase 3 trial of pamrevlumab , an experimental therapy from FibroGen to treat idiopathic pulmonary fibrosis (IPF), failed to meet its primary goal of slowing lung function decline. (pulmonaryfibrosisnews.com)
  • Visit the Pulmonary Fibrosis News forums to connect with others in the PF community. (pulmonaryfibrosisnews.com)
Inflammation10
Pamrevlumab4
  • Pamrevlumab binds to CTGF and may prevent this cascade. (parentprojectmd.org)
  • Targeting CTGF is a clinically validated treatment approach for IPF, as shown by trial data from the intravenously delivered monoclonal antibody pamrevlumab. (bignewsnetwork.com)
  • Previously reported preclinical data for PRS-220 demonstrated superior on-target potency compared to pamrevlumab, an intravenously infused CTGF antagonist in late-stage clinical development. (bignewsnetwork.com)
  • By blocking CTGF activity, pamrevlumab was expected to reduce the buildup of scar tissue and ease disease symptoms . (pulmonaryfibrosisnews.com)
Cystic fibrosis2
  • In February 2018, the U.S. Food and Drug Administration (FDA) approved Vertex Pharmaceuticals' SYMDEKO (tezacaftor/ivacaftor and ivacaftor) for the treatment of cystic fibrosis (CF) in people age 12 and older with certain mutations. (medgadget.com)
  • Pancreatic Insufficiency in Cystic Fibrosis: Influence of Inflammatory Response Genes. (cdc.gov)
Liver fibrosis6
  • Cohort and case-control studies reported an inverse association between coffee consumption and the degree of liver fibrosis as well as the development of liver cancer. (mdpi.com)
  • Almost all studies highlighted the beneficial effects of this beverage against liver fibrosis with the most solid results indicating a pivot role for both caffeine and chlorogenic acids. (mdpi.com)
  • Furthermore, growing research collaboration among the key players to develop novel treatment regime combined with regulatory approval of underline drugs for treatment of liver fibrosis is expected to drive the market growth in near future. (medgadget.com)
  • The global liver fibrosis treatment market is expected to grow at 10.8% CAGR over the forecast period, owing to increasing prevalence of risk factors affecting liver fibrosis, worldwide. (medgadget.com)
  • Among treatment type, hepatotropic drug accounted for significant market share in liver fibrosis treatment market, as it enables safe and efficient treatment for reducing fibrosis in patients. (medgadget.com)
  • Among end users, hospitals segment is expected to account for major market share during the forecast period, as hospital offer primary treatment option for patient suffering with liver fibrosis. (medgadget.com)
Cardiac fibrosis21
  • Cardiac fibrosis is a hallmark of numerous chronic cardiovascular diseases that leads to heart failure. (hindawi.com)
  • Dysregulation of microRNAs has been confirmed to be involved in cardiac fibrosis development. (hindawi.com)
  • This study was the first to highlight the role and molecular mechanism of miR-409-3p in cardiac fibrosis. (hindawi.com)
  • Furthermore, myocardial infarction surgery-induced cardiac fibrosis and dysfunction were attenuated by systemic delivery of miR-409-3p antagomir. (hindawi.com)
  • Gpd1 siRNA abolished the antifibrotic effect of miR-409-3p inhibitor in neonatal rat cardiac fibroblasts, suggesting that miR-409-3p promotes cardiac fibrosis at least partially through Gpd1. (hindawi.com)
  • Moreover, GATA2 was identified as a cardiac fibrosis-associated upstream positive transcription factor of miR-409-3p. (hindawi.com)
  • Finally, these findings suggest that modulating miR-409-3p could be a potential therapeutic method for cardiac fibrosis. (hindawi.com)
  • Cardiac fibrosis is a pathological manifestation of myocardial remodeling, which is characterized by increased fibroblast-to-myofibroblast conversion and excessive extracellular matrix (ECM) deposition within the myocardial interstitium, leading to myocardial stiffness, ventricular dilation, arrhythmias, and heart failure [ 1 , 2 ]. (hindawi.com)
  • Understanding the molecular mechanisms underlying cardiac fibrosis is beneficial to the development of novel strategies for therapeutic intervention. (hindawi.com)
  • Accumulating studies have revealed that miRNAs that participate in the myocardial fibrotic program, such as miR-18a-5p, attenuate cardiac fibrosis via regulating the Notch2 pathway [ 13 ], and miR-24-3p alleviates myocardial fibrosis through PHB2 [ 14 ]. (hindawi.com)
  • These observations demonstrated that miRNAs might be promising therapeutic targets for alleviating cardiac fibrosis. (hindawi.com)
  • For instance, miR-409-3p promotes epithelial to mesenchymal transition and tumor growth in prostate cancer and also accelerates osteoblastic differentiation through the Wnt/ β -catenin pathway [ 17 , 18 ], a crucial pathway in regulating cardiac fibrosis. (hindawi.com)
  • Endothelial-to-mesenchymal transition (EndMT) is an important mechanism underlying cardiac fibrosis. (dovepress.com)
  • This study aimed to investigate the possible effect of TMZ on cardiac fibrosis exerted via the inhibition of NOX2-mediated EndMT. (dovepress.com)
  • A cardiac fibrosis model was established in Sprague-Dawley rats through a subcutaneous injection of isoproterenol (ISO, 5 mg/kg/d). (dovepress.com)
  • Rats injected with ISO exhibited severe interstitial cardiac fibrosis and perivascular fibrosis, decreased left ventricular ejection fraction, and increased NOX activity. (dovepress.com)
  • TMZ treatment mitigated cardiac fibrosis, ameliorated left ventricular dysfunction, and reduced NOX activity. (dovepress.com)
  • TMZ may ameliorate EndMT and ISO-induced cardiac fibrosis through the NOX2/NF-κB/Snail pathway. (dovepress.com)
  • The findings of the study may provide new insights into the potential role of TMZ in the pathophysiology of cardiac fibrosis. (dovepress.com)
  • Recently, EndMT has been increasingly recognized as a vital process that contributes to various cardiovascular pathologies in adults, which include atherosclerosis, valvular heart disease, cardiac fibrosis, and myocardial infarction. (dovepress.com)
  • Yin Yang 1 Suppresses Dilated Cardiomyopathy and Cardiac Fibrosis Through Regulation of Bmp7 and Ctgf . (bvsalud.org)
Collagen10
  • Collagen content was measured by Sircol method, and fibrosis marker levels were detected by PCR and Western Blot. (researchsquare.com)
  • Myocardial fibrosis, characterized as interstitial fibroblast proliferation and excessive collagen deposition, is the structural basis of myocardial stiffness and the key process of cardiac function transformation from the compensatory phase to heart failure. (dovepress.com)
  • an upstream modulator of CTGF and collagen), in rats performing one of two repetitive tasks, with or without anti-inflammatory drugs. (cdc.gov)
  • Immunohistochemistry confirmed PCR results, and also showed greater increases of CTGF and collagen matrix in 9-week HRHF rats than 9-week HRNF rats. (cdc.gov)
  • We found that fibrocytes respond to fibrogenic stimuli (AngII and CTGF) by increasing the expression of collagen and CTGF, an early molecular mediator of fibrosis, while also promoting fibrocyte differentiation. (dal.ca)
  • JNK inhibitor significantly inhibited CTGF collagen and fibronectin We manifestation induced by TGF-β1 in THSF. (bio2009.org)
  • TGF-β1 performed an important part in the activation of quiescent corneal keratocytes [15] CTGF was induced by TGF-β1 and mediated the result of TGF-β1 on collagen fibronectin synthesis [16]. (bio2009.org)
  • Antisense oligonucleotides and neutralizing antibodies to CTGF reduce TGF-β1 induced collagen synthesis cell proliferation and matrix contraction in corneal fibroblast [17] [18]. (bio2009.org)
  • Inhibition of p38 could suppress collagen MifaMurtide We and CTGF expression induced by TGF-β1 in conjunctival fibroblasts [28] fibronectin. (bio2009.org)
  • Our Previous research show that TGF-β1 induced the activation of JNK in corneal fibroblast inhibition of JNK pathway can efficiently inhibit TGF-β1 induced CTGF manifestation and following corneal fibroblast proliferation and collagen over-expression in corneal fibroblasts [15]. (bio2009.org)
Monoclonal Antibody1
  • The poster will be presented on May 21, 2023, from 11:30 AM to 1:15 PM (Session A67, P1052) and demonstrates that PRS-220 achieved proof of concept in a silica-induced lung fibrosis mouse model when delivered to the lung by inhalation and outperformed a systemically administered CTGF-targeting monoclonal antibody, reinforcing the transformative potential of a local intervention in this pathway. (bignewsnetwork.com)
Fibrotic3
Renal8
  • Moreover, we interestingly found overlaps of pathways between renal fibrosis and skin fibrosis, such as GO:1901890-positive regulation of cell junction assembly, as well as common regulatory genes, such as CTGF, which is the key molecule regulating fibrogenesis. (frontiersin.org)
  • The cause of late renal allograft loss, once known as chronic allograft nephropathy, has been renamed "interstitial fibrosis and tubular atrophy" (IF/TA) to reflect the histologic pattern seen on biopsy. (biomedcentral.com)
  • Inhibiting intrinsic renal pathways associated with irritation (NADPH oxidase) and fibrosis (Smads, TGF-, and CTGF) might verify beneficial. (ap26113.com)
  • The part of TGF- in renal fibrosis Robust evidence suggests that essentially all progressive forms of CKD are characterized by marked build up of extracellular matrix proteins in the glomerulus and tubulointerstitium. (ap26113.com)
  • Renal fibrosis is the final common manifestation defining CKD and is characterized by progressive tissue scarring that leads to glomerulosclerosis and tubulo interstitial fibrosis.10 Although the precise sequence of molecular events that result in renal fibrosis has not been completely elucidated, present data indicate that TGF- is the expert regulator of this process. (ap26113.com)
  • to investigate the effect of Trip on renal interstitial fibrosis in a model of unilateral ureteral obstruction (UUO). (vegfrinhibitors.com)
  • Conclusion: Trip significantly attenuated tubulointerstitial fibrosis in a rat UUO model and the effect of Trip on renal Sulfite dehydrogenase fibrosis was similar to that of MMF. (vegfrinhibitors.com)
  • of renal fibrosis. (vegfrinhibitors.com)
Pathways4
  • The signaling pathways linking angiotensin II to CTGF formation are, however, incompletely understood. (amrita.edu)
  • kidney energy sensing pathways (AMPK, sirtuins, and mTOR) Delamanid inhibitor in a variety of kidney diseases and how they are linked to swelling and fibrosis. (ap26113.com)
  • SMAD MifaMurtide proteins will be the major substrates of TGF-β1 receptors [19] whereas we previously discovered that TGF-β1 up-regulated CTGF manifestation had not been via SMAD pathways in rabbit corneal wound curing [14]. (bio2009.org)
  • Predicated on these results it had been hypothesized that MAPK pathways could mediate CTGF manifestation and corneal skin damage in corneal wound curing. (bio2009.org)
Pathologic3
  • Thus, cyclic RGD peptides are powerful multifunctional ligands for both addressing nanomaterials to the TM and interfering with pathologic CTGF signaling upon arrival. (uni-regensburg.de)
  • From this data, we propose that fibrocytes are a key effector cell that directly promotes pathologic fibrosis within the injured myocardium. (dal.ca)
  • The pathologic hallmark of scleroderma is progressive fibrosis of tissues. (medscape.com)
Promotes1
  • Using an anti-hypertension treatment, we found that hypertension as a physiologic stimulus likely promotes cellular infiltration and corresponding fibrosis. (dal.ca)
Dysfunction3
  • Fibrosis is characterized by an excessive accumulation of extracellular matrix components which could result in tissue dysfunction. (springer.com)
  • Key Results: In vivo, administration of the mAb alleviated doxorubicin-induced cardiac dysfunction and fibrosis. (unito.it)
  • Four weeks post-surgery, CRA-treated mice developed blunted cardiac hypertrophy, fibrosis, and dysfunction, and showed increased LC3 II and p-AMPK expression. (silverchair.com)
Mechanisms2
  • We hope to offer a new insight into the cellular and molecular mechanisms underlying fibrosis and therefore help leading to the development of new drugs, which specifically delay or even improve the symptoms of fibrosis. (frontiersin.org)
  • 1 Thus, it is imperative to understand the mechanisms involved in inhibition of myocardial fibrosis. (dovepress.com)
Mechanism1
Progressive fibrosis1
  • As progressive fibrosis might be a traveling push for the disruption of glomerular and tubular architecture, inhibition of the major mediators responsible for matrix build up might sluggish or arrest the progression of CKD. (ap26113.com)
Protein3
  • CTGF is a matricellular protein that is involved in ECM production and remodeling. (wikipedia.org)
  • Treatment resulted in a statistically significant reduction of CTGF mRNA and protein at the treatment site, with no significant toxicity or adverse effects. (bmj.com)
  • We also established that treatment with activated protein C (aPC) conferred protection against the development of myocardial fibrosis, potentially by inhibiting fibrocyte recruitment and/or activation. (dal.ca)
Expression4
  • The present study explored whether SGK1 is transcriptionally regulated by angiotensin II and participates in the angiotensin II-dependent regulation of CTGF expression. (amrita.edu)
  • Echocardiographic parameters, myocardial fibrosis, NOX2 expression and EndMT were assessed. (dovepress.com)
  • Quantitative PCR (qPCR) analyses of HRNF muscles showed increased expression of Col1 in weeks 3-9, and CTGF in weeks 6 and 9. (cdc.gov)
  • MMF or Trip significantly reduced the mRNA expression of TGF-β1, CTGF, MCP-1 and osteopontin. (vegfrinhibitors.com)
Myocardial infarction1
  • Myocardial fibrosis occurs in almost all chronic cardiovascular diseases [ 3 ], such as myocardial infarction (MI), which remains a leading cause of morbidity and mortality worldwide [ 4 ]. (hindawi.com)
Pathological1
  • Myocardial fibrosis is a common pathological finding in patients with cardiovascular disease and is believed to be a major contributing factor in the development of end stage organ failure. (dal.ca)
Hypoxia1
  • the effects of hypoxia and fibrosis may also play a role in obesity complications via notably ectopic-lipid accumulation in non-adipocyte cells. (springer.com)
Vitro2
  • Methods PH-109 mediated mRNA silencing of CTGF was validated in 4T1 cells in vitro by RT-qPCR. (bmj.com)
  • Results PH-109 provided concentration-associated silencing of CTGF in vitro. (bmj.com)
Vascular1
Tissue Repair1
  • CTGF orchestrates diverse multicellular processes including embryonic development, wound healing, and tissue repair. (bmj.com)
Manifestation8
  • In corneal wound curing the JNK inhibitor considerably inhibited CTGF manifestation markedly improved the structures of corneal stroma and decreased corneal scar development but didn't possess a measurable effect on corneal wound curing in vivo. (bio2009.org)
  • Our outcomes indicate that JNK mediates the manifestation of CTGF and corneal skin damage in corneal wound curing and might be looked at as specific focuses on of medication therapy for corneal skin damage. (bio2009.org)
  • We've previously demonstrated that manifestation MifaMurtide of TGF-β1 and CTGF improved significantly during corneal wound curing TGF-β1 could induce CTGF manifestation in vivo [14]. (bio2009.org)
  • This is consistent with additional reports where TGF-β1 improved CTGF manifestation in human being corneal fibroblasts [12]. (bio2009.org)
  • Consequently understanding systems regulating manifestation of CTGF improved by TGF-β1 can be of great importance to inhibit corneal skin damage. (bio2009.org)
  • There is certainly proof that TGF-β1 induced CTGF manifestation can be mediated through JNK in human being lung fibroblasts [25]. (bio2009.org)
  • In gingival fibroblasts the only real MAPK mediates the TGF-β1 activated CTGF manifestation was JNK [26]. (bio2009.org)
  • ERK mediates TGF-β1 induced CTGF manifestation in pores and skin fibroblasts [27]. (bio2009.org)
Inhibition1
  • CTGF-inhibition has shown promise in decreasing metastatic dissemination and sensitizing to cancer cells to chemotherapy in preclinical models. (bmj.com)
Biomarker1
  • For instance, in April 2017, Bristol-Myers Squibb Company and Nordic Bioscience signed a collaboration agreement for development of biomarker technology to potentially diagnose and monitor fibrosis disease including Non-alcoholic steatohepatitis (NASH). (medgadget.com)
Effector1
  • Cardiac fibroblasts are generally the primary effector cells of fibrosis and have been reported to be partly derived from cardiac endothelial cells through the endothelial to mesenchymal transition (EndMT) process. (dovepress.com)
Pathogenesis2
  • Fibrosis can affect chronic graft rejection, tumor invasion and metastasis, and the pathogenesis of many progressive myopathies. (frontiersin.org)
  • Background: Transforming growth factor-beta (TGF-β) plays a central role in the pathogenesis of oral submucous fibrosis (OSF). (ntu.edu.tw)
Wound1
  • Nevertheless the signaling pathway of CTGF creation in corneal wound curing remains unclear. (bio2009.org)
Significantly1
  • Fibrosis markers were more significantly reduced in the hUC-MSCs + PFD relative to the PFD alone group and the hUC-MSCs group. (researchsquare.com)
Cellular2
  • Rapid cellular infiltration into the cardiac tissue is evident in fibrosis but the infiltrating populations and their functions have yet to be completely elucidated. (dal.ca)
  • The aim of this thesis was to characterize the phenotype and function of this cellular population in a model of hypertension mediated myocardial fibrosis. (dal.ca)
Inhibit1
  • Understanding their migration and function is therefore essential to the development of future therapies targeting this cell type to inhibit their role in fibrosis. (dal.ca)
Diseases1