• Diabetic cardiomyopathy (DCM), a substantial contributor to morbidity and mortality in diabetics, is seen as a ventricular dysfunction, within the lack of coronary atherosclerosis and hypertension. (researchassistantresume.com)
  • Non-ischemic cardiomyopathy (NICM) can cause left ventricular dysfunction through interstitial fibrosis, which corresponds to the failure of cardiac tissue remodeling. (nature.com)
  • Among cardiac macrophage subtypes, WWP2 dysfunction primarily affects Ly6c high monocytes via modulating Ccl5, and consequentially macrophage infiltration and activation, which contributes to reduced myofibroblast trans -differentiation. (nature.com)
  • TMZ treatment mitigated cardiac fibrosis, ameliorated left ventricular dysfunction, and reduced NOX activity. (dovepress.com)
  • Many evidences indicated that cardiac fibroblasts proliferation and extreme extracellular matrix (ECM) deposition induced myocardial fibrosis and added to ventricular dysfunction ventricular dilation and center failing [1]. (hiv-proteases.com)
  • In selected patients affected by HF and severe dysfunction of left ventricle ejection fraction (LVEF), with left bundle brunch block, the cardiac resynchronization therapy with a defibrillator (CRT) is the treatment of choice to improve symptoms, NYHA class, and quality of life. (hindawi.com)
  • Oxidative stress and mitochondrial dysfunction are important mechanisms of ventricular remodeling, predisposed to the development of diabetic cardiomyopathy (DCM) in type 2 diabetes mellitus. (mdpi.com)
  • Collagen remodeling and cardiac dysfunction in patients with hypertrophic cardiomyopathy: the significance of type III and VI collagens. (pitt.edu)
  • Ventricular hypertrophy and/or dilatation are main structural changes that reflect a pathological response of the heart, accompanied by molecular and cellular changes that functionally translate into diastolic and/or systolic dysfunction [ 7 ]. (biomedcentral.com)
  • Areas covered: This article reviews the outpatient pharmacological management of chronic HF due to left ventricular systolic dysfunction and offers recommendations on the use of various drugs. (docksci.com)
  • The aim of this review is to provide an update on the pharmacological interventions indicated in the outpatient management of HF due to left ventricular (LV) systolic dysfunction. (docksci.com)
  • Heart failure with preserved ejection fraction (HFpEF) Heart failure (HF) is a syndrome of ventricular dysfunction. (msdmanuals.com)
  • Energy starvation in hypertrophied cardiomyocytes is believed to occur as a result of a combination of factors, such as the reduction in the ratio in the surface area between capillaries and cardiomyocytes and increased myocyte diameter, see Figure 1 3 . (europeanpharmaceuticalreview.com)
  • Alveoli, pulmonary vessels, α -smooth muscle actin content in pulmonary arterioles, size of cardiomyocytes, right to left ventricular wall diameter ratio, and endothelin-1 plasma concentrations were assessed. (biomedcentral.com)
  • IGF-1 release induced higher levels of Akt phosphorylation and hypertrophy in cardiomyocytes resulting in increased force generation of EHM. (uni-goettingen.de)
  • Collectively, these results indicate the potential for therapeutic alteration of cell fate decisions and pathological gene regulatory networks by GATA4-targeted compounds modulating chamber-specific transcriptional programs in multipotent cardiac progenitor cells and cardiomyocytes. (biomedcentral.com)
  • In addition, In vitro cell culture models will be studied to address the underlying cellular mechanisms by utilizing: 1) Adult mouse cardiac fibroblasts (F2KO and WT) and 2) Neonatal rat ventricular cardiomyocytes. (centerforpediatricresearch.org)
  • We quantified CXCL10 in human CKD plasma and tested the response of human iPSC-derived cardiomyocytes and primary cardiac fibroblasts to serum from CKD donors. (biomedcentral.com)
  • In humans, we found increased plasma CXCL10 concentrations in advanced CKD, and identified the production of CXCL10 in cardiomyocytes and cardiac fibroblasts. (biomedcentral.com)
  • There is a growing body of evidence which demonstrates that following ACS, microRNAs might inhibit fibroblast proliferation and scarring, as well as harmful apoptosis of cardiomyocytes, and stimulate fibroblast reprogramming into induced cardiac progenitor cells. (archivesofmedicalscience.com)
  • Excessive stimulation of this receptor causes pathological proliferation of cardiac valve fibroblasts, with chronic overstimulation leading to valvulopathy. (wikipedia.org)
  • RA signaling continues to be implicated within the legislation of cell differentiation, proliferation and apoptosis [116,117], and a considerable body of understanding has gathered on its function in the legislation of cardiomyocyte development, apoptosis and mobile function in response to different pathophysiological stimuli. (researchassistantresume.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)
  • We found that reduced kidney function resulted in the expansion of cardiac macrophages, in particular through local proliferation of resident populations. (biomedcentral.com)
  • Ang II binds to AT 1 R, which can induce vasoconstriction, increase blood pressure, and further induce cardiac hypertrophy and proliferation of fibroblasts [15]. (researchsquare.com)
  • Cardiomyocyte hypertrophy is a mechanism by which myocardial mass is increased to compensate for any elevated physical demands placed upon the heart, thus ensuring that adequate perfusion of body tissues is maintained during these periods. (europeanpharmaceuticalreview.com)
  • On the mobile level, cardiac redecorating is seen as a cardiomyocyte hypertrophy, fibroblast hyperplasia associated with a rise in collagen deposition inside the interstitial matrix (fibrosis) and cell loss of life. (researchassistantresume.com)
  • Due to cellular heterogeneity in the heart, the activation of gene programs representing specific atrial and ventricular cardiomyocyte subtypes would be highly desirable. (biomedcentral.com)
  • Keywords: Puerarin monocyte chemoattractant proteins (MCP-1) transforming development element-β1 (TGF-β1) cardiac fibrosis myocardial infarction (MI) Intro Maladaptive pathological adjustments lead to center failing in the cardiac redesigning procedure after myocardial infarction (MI) including cardiomyocyte hypertrophy improved swelling and fibrosis. (hiv-proteases.com)
  • In this review, we focus on the role of cardiomyocyte-derived and cardiac fibroblast-derived microRNAs that are involved in the regulation of genes associated with cardiomyocyte and fibroblast function and in atherosclerosis-related cardiac ischemia. (archivesofmedicalscience.com)
  • The 5-HT2B receptor subtype is involved in: CNS: inhibition of serotonin and dopamine uptake, behavioral effects Vascular: pulmonary vasoconstriction Cardiac: The 5-HT2B receptor regulates cardiac structure and functions, as demonstrated by the abnormal cardiac development observed in 5-HT2B receptor null mice. (wikipedia.org)
  • Macitentan treatment significantly increased pulmonary vessel count (p = 0.004) and decreased right to left ventricular wall diameter ratios (p = 0.002). (biomedcentral.com)
  • Therefore, an intervention at the ET-1 receptor level might have a positive effect on pulmonary vascular resistance and right ventricular remodelling. (biomedcentral.com)
  • TOF is a congenital heart anomaly which consists of pulmonary stenosis, ventricular septal defect, dextroposition of the aorta (aorta is on the right side instead of the left) and hypertrophy of the right ventricle. (betalifesci.com)
  • For instance, C57BL/6J mice are resistant to hepatic, renal and cardiac fibrosis but susceptible to pulmonary and intestinal fibrosis. (biomedcentral.com)
  • Worsened right ventricular remodeling in males was independent of pulmonary congestion. (biomedcentral.com)
  • Pulmonary arterial hypertension (PAH) is a lethal vasculopathy characterized by pathogenic remodeling of pulmonary arterioles leading to increased pulmonary pressures, right ventricular hypertrophy, and heart failure. (biomedcentral.com)
  • Severe pulmonary hypertension leads to right ventricular overload and failure. (msdmanuals.com)
  • Surprisingly, however, 5-HT2B receptor activation appears to be protective against the development of serotonin syndrome following elevated extracellular serotonin levels, despite its role in modulating serotonin release. (wikipedia.org)
  • Meschiari CA, Ero OK, Pan H, Finkel T, Lindsey ML. The impact of aging on cardiac extracellular matrix. (pitt.edu)
  • Lindsey ML, Hall ME, Harmancey R, Ma Y. Adapting extracellular matrix proteomics for clinical studies on cardiac remodeling post-myocardial infarction. (pitt.edu)
  • If myocytes are lost due to injury, the myocardium is unable to restore its myocyte content and instead undergoes compensatory hypertrophy and remodeling. (uni-goettingen.de)
  • Intramyocardial fibroblast myocyte communication. (ac.ir)
  • Importance of myocyte-nonmyocyte interactions in cardiac development and disease. (ac.ir)
  • Cardiac myocyte-derived follistatin-like 1 prevents renal injury in a subtotal nephrectomy model. (ac.ir)
  • Cardiac myocyte follistatin-like 1 functions to attenuate hypertrophy following pressure overload. (ac.ir)
  • It inhibits myoblast differentiation and enhances fibroblast growth factor-induced angiogenesis. (betalifesci.com)
  • Considering the results of VEGF and vascular histology, the physiological effects of NDNF on the induction of cardiac angiogenesis in healthy subjects with exercise training need further studies. (ac.ir)
  • Despite the fact that the hypertrophied myocardium is initially capable of maintaining adequate blood flow to body tissues and organs, if this growth persists, the enlarged heart muscle progresses to an irreversible failing or de-compensated state1. (europeanpharmaceuticalreview.com)
  • Cardiac tissue engineering aims to recreate and provide functional myocardium that replaces the injured myocardium. (uni-goettingen.de)
  • To generate large myocardium capable of encompassing the ventricles, a novel process to systematically upscale the dimensions of engineered myocardium to a humanized Biological Ventricular Assisted Device (hBioVAD) was introduced. (uni-goettingen.de)
  • Finally, we measured the level of Ca 2+ by microplate method and the protooncogene c-fos and c-myc mRNA in left ventricular myocardium by qRT-PCR. (researchsquare.com)
  • decrease the expression of β-MHC, ANF, Ang II, AT 1 R, c-fos and c-myc mRNA and the protein levels of PLC, IP 3 , AngII and AT 1 R in left ventricular myocardium, in addition, the content of Ca 2+ also decrease. (researchsquare.com)
  • Hypertrophic cardiomyopathy (HCM) is a common inherited heart disease with serious adverse outcomes, including heart failure, arrhythmias, and sudden cardiac death. (rupress.org)
  • If we allow this to continue, the results may lead to ventricular remodeling, decompensation of cardiac function and dilated cardiomyopathy, heart failure and even sudden cardiac death[7] Therefore, preventing the occurrence and development of cardiac hypertrophy is very important. (researchsquare.com)
  • Rats injected with ISO exhibited severe interstitial cardiac fibrosis and perivascular fibrosis, decreased left ventricular ejection fraction, and increased NOX activity. (dovepress.com)
  • If left untreated, cardiac hypertrophy will eventually progress to heart failure (HF), a condition where the heart is no longer able to pump enough blood to meet the body's needs. (adinstruments.com)
  • PV Loops are generated by inserting a pressure-volume catheter into the left or right ventricle of the heart and plotting the real-time ventricular pressure against ventricular volume over a complete cardiac cycle. (adinstruments.com)
  • A typical series of left ventricular PV Loops displayed in LabChart . (adinstruments.com)
  • FGF23 elevation and left ventricular hypertrophy in mice with chronic kidney disease. (tamu.edu)
  • Mancuso P, Rahman A , Hershey S.D., Dandu L, Nibbelink K.A., Simpson R.U. (2008) 1,25-Dihydroxyvitamin-D3 treatment reduces cardiac hypertrophy and left ventricular diameter in spontaneously hypertensive heart failure-prone (cp/+) rats independent of changes in serum leptin. (wsu.edu)
  • Prevalence, clinical profile, and significance of left ventricular remodeling in the end-stage phase of hypertrophic cardiomyopathy. (pitt.edu)
  • Fibroblast growth factor-23 (FGF23) has been associated to left ventricular (LV) hypertrophy and heart failure (HF) severity. (biomedcentral.com)
  • We observed that cigarette smoking exacerbated both left and right ventricular remodeling only in males at an early stage of post-MI. (biomedcentral.com)
  • CS-exposed males exhibited enhanced increases in left ventricular end systolic and diastolic volumes, as well as reductions in ejection fraction and fractional area changes of left ventricular base. (biomedcentral.com)
  • Left ventricular (LV) failure causes shortness of breath and fatigue, and right ventricular (RV) failure causes peripheral and abdominal. (msdmanuals.com)
  • However, pathological conditions can disrupt this intricate mechanosensory system and manifest as potentially life-threatening cardiac arrhythmias. (mdpi.com)
  • Adjustments in RA homeostasis (missing or more than RA) bring about serious malformations during cardiogenesis, recommending that a specific tissue focus of RA can be indispensable for the correct induction of signaling pathways very important to regular myocardial cell development and differentiation in early embryonic levels. (researchassistantresume.com)
  • Measured by the ability of the immobilized protein to enhance BMP2-induced alkaline phosphatase activity in C3H10T1/2 mouse embryonic fibroblast cells.The ED50 for this effect is typically 4-20 ug/mL. (betalifesci.com)
  • A tight spatial and timing regulation of growth factor action during embryonic development has been suggested [4]. (unicyte.ch)
  • The aim of this study was to investigate the effect and mechanism of Leonurine (Leo) against pressure-overload cardiac hypertrophy induced by abdominal aortic constriction (AAC) in rats. (researchsquare.com)
  • Previous studies have shown that its development is closely related to cardiac overload[6], so abdominal aortic constriction(AAC) can use this principle to establish model of myocardial hypertrophy. (researchsquare.com)
  • Chemical compounds that modulate atrial and ventricular cell fate could be used to improve subtype-specific differentiation of endogenous or exogenously delivered progenitor cells in order to promote cardiac regeneration. (biomedcentral.com)
  • In patients under optimal medical therapy with moderate to severe HF and cardiac dyssynchrony, cardiac resynchronization therapy (CRT) with a defibrillator improves contractile function and reverse ventricular remodeling, ameliorating symptoms, quality of life (QoL), and clinical outcomes [ 7 , 8 ]. (hindawi.com)
  • Clinical presentation, long-term follow-up and outcomes of 1001 arrhythmogenic right ventricular dysplasia/cardiomyopathy patients and family members // Circulation: Cardiovascular Genetics. (vitapol.com.ua)
  • Recent evidence implicates monocytes/macrophages in the etiopathology of cardiac fibrosis, but giving their heterogeneity and the antagonizing roles of macrophage subtypes in fibrosis, targeting these cells has been challenging. (nature.com)
  • The results shown that puerarin could inhibit the recruitment and activation of monocytes/macrophages reduce the manifestation of TGF-β1 in the cardiac cells and consequently considerably attenuated cardiac fibrosis after MI. (hiv-proteases.com)
  • Macrophages are known to be involved in both chronic kidney disease (CKD) and heart failure, however their role in the development of cardiorenal syndrome is less clear. (biomedcentral.com)
  • We thus sought to investigate the role of macrophages in uremic cardiac disease. (biomedcentral.com)
  • However, whether macrophages participate in the development of cardiorenal syndrome is less clear. (biomedcentral.com)
  • Here we focus on WWP2, an E3 ubiquitin ligase that acts as a positive genetic regulator of human and murine cardiac fibrosis, and show that myeloid specific deletion of WWP2 reduces cardiac fibrosis in hypertension-induced NICM. (nature.com)
  • Reperfusion after cardiac ischemia increases cell death and infarct size (IS), called myocardial ischemia/reperfusion (I/R) injury, which is the main cause of myocardial injury during the cardiac surgery particularly in coronary artery bypass graft surgery ( 1 , 2 ). (spandidos-publications.com)
  • Endothelial-to-mesenchymal transition (EndMT) is an important mechanism underlying cardiac fibrosis. (dovepress.com)
  • 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)
  • During embryogenesis endothelial cells exhibit substantial plasticity that contribute to cardiac development by undergoing endothelial-to-mesenchymal transition (EndoMT). (surrey.ac.uk)
  • The current treatment options for controlling hypertrophic growth involve targeting the extra-cardiac factors, such as high blood pressure. (adinstruments.com)
  • While this may be an effective treatment for some people, there are no clinically available treatment options that target the intra-cardiac factors mediating hypertrophic growth. (adinstruments.com)
  • Earlier intensive studies possess taken notice TEI-6720 of the TGF-β-induced ECM and fibrosis in a variety of illnesses including cardiac fibroblast-myofibroblast changeover [7 11 TGF-β1 function was mediated by TGF-β type I and type II receptors. (hiv-proteases.com)
  • In humans, a number of genetic factors have been linked to the development of fibrosis in a variety of different organs. (biomedcentral.com)
  • One complementary therapy could be 're-activating' vasculogenesis (i.e. the differentiation of precursor cells into mature endothelial cells), a mechanism that occurs in the heart during development but is quiescent in adult hearts. (elifesciences.org)
  • Retinoid Receptor-Mediated Signaling in Cardiac Redecorating Cardiac remodeling includes a main role within the development to HF, that is associated with modifications within the ventricular framework and function, caused by myocardial damage, pressure or quantity overload. (researchassistantresume.com)
  • Following myocardial injury and/or mechanical overload, the heart can initially maintain cardiac output by enhancing intrinsic compensatory capacity. (centerforpediatricresearch.org)
  • AT 1 R is a member of the 7-fold transmembrane G-protein-coupled receptor (GPCR) family[12,13], mainly exists in the myocardial membrane and can mediate cardiac hypertrophy induced by pressure overload and mechanical stimulation after activation [14]. (researchsquare.com)
  • Here, we hypothesized that inhibit RAS may improve ACC rats anti hypertrophy caused by stress overload. (researchsquare.com)
  • Additional paracrine functionality was integrated by generating insulin-like growth factor-1 (IGF-1) secreting fibroblasts for tissue engineering applications. (uni-goettingen.de)
  • Akins RE, Gratton K, Quezada E, Rutter H, Tsuda T, Soteropoulos P. Gene expression profile of bioreactor-cultured cardiac cells: Activation of morphogenetic pathways for tissue engineering. (centerforpediatricresearch.org)
  • Nuclear Smad2/3 complex activates transcription of α-SMA and collagen I [12 13 In addition fibrosis typically results from simultaneous chronic inflammation tissue remodeling during repair processes [14 15 Therefore therapies that target the inflammatory response or TGF-β1 signaling pathways might effectively attenuate the progression of fibrosis in cardiac remodeling. (hiv-proteases.com)
  • We also point out a possible contribution of adipose tissue-associated mast cell secre- tory activity to the development of these diseases. (123dok.org)
  • METHODS: UMR106 cells and isolated neonatal rat ventricular myocytes (NRVM) were treated with ketone body ß-hydroxybutyrate. (bvsalud.org)
  • JAG1/Jagged 1 seems to be involved in early and late stages of mammalian cardiovascular development. (betalifesci.com)
  • Dr. Min Zi , a Researcher in the Division of Cardiovascular Sciences at Manchester University (UK), is one such scientist who is actively investigating these intra-cardiac factors. (adinstruments.com)
  • During chronic kidney disease (CKD), alterations in bone and mineral metabolism include increased production of the hormone fibroblast growth factor 23 (FGF23) that may contribute to cardiovascular mortality. (tamu.edu)
  • Myocardial hypertrophy occurs in many cardiovascular diseases. (researchsquare.com)
  • Myocardial hypertrophy is one of the important causes of death of patients caused by cardiovascular diseases and an independent risk factor for the morbidity and mortality of cardiovascular diseases [1-3]. (researchsquare.com)
  • Atherosclerotic plaque rupture is the leading cause of cardiovascular death resulting from acute coronary syndrome (ACS) and leads to cardiac remodeling and fibrosis following ACS. (archivesofmedicalscience.com)
  • Several etiologies with distinct mechanisms ultimately bring about signs of heart exhaustion such as reduced ejection fraction, reduced compliance and ventricular dilatation. (pitt.edu)
  • Kato S, Spinale FG, Tanaka R, Johnson W, Cooper Gt, Zile MR. Inhibition of collagen cross-linking: effects on fibrillar collagen and ventricular diastolic function. (pitt.edu)
  • Recently several reporters demonstrated it had healing and anti-fibrotic effects on cardiac remodeling through its anti-inflammatory anti-oxidant effects [20 22 In TEI-6720 light of above points we supposed that puerarin could abolish cardiac fibrosis by inhibition of TGF-β1 signaling pathways and inflammatory responds. (hiv-proteases.com)
  • Whole-genome studies have provided a useful insight into how gene patterns may influence the development and/or progression of certain pathological pathways, including fibrosis [ 2 ]. (biomedcentral.com)
  • Biomarkers, Socioeconomic Factors, and Right Ventricular Function After Surgical Repair for Tetralogy of Fallot. (stanford.edu)
  • The aim of this narrative review is to summarize contemporary evidence on the use of circulating cardiac biomarkers of heart failure (HF) and to identify a promising biomarker model for clinical use in personalized point-of-care HF management. (annlabmed.org)
  • These receptors are also overexpressed in human failing heart and antagonists of 5-HT2B receptors were uncovered to prevent both angiotensin II or beta-adrenergic agonist-induced pathological cardiac hypertrophy in mouse. (wikipedia.org)
  • Although these in vivo models have provided a useful means of studying the factors involved in this cardiac condition in the whole heart. (europeanpharmaceuticalreview.com)
  • in offering the impetus for producing novel therapeutic methods for the avoidance and treatment of diabetes-induced cardiac problems and heart failing. (researchassistantresume.com)
  • Furthermore, it is unknown whether endogenous progenitors/stromal cells in the adult human heart could be chemically induced to generate functional atrial or ventricular heart muscle to treat adult heart diseases. (biomedcentral.com)
  • Mechanoelectric feedback provides a rapid mechanism for detecting even subtle changes in the mechanical environment and transducing these signals into electrical responses, which can adjust a variety of cardiac parameters such as heart rate and contractility. (mdpi.com)
  • Sponsor(s): National Heart, Lung, and Blood Institute( NHLBI) investigator - heart: To develop a acid hypothesis of second development syndrome( CHF). (hone.world)
  • At least eight novel pediatric candidate genes carrying de novo variants have plausible roles in lung/heart development. (biomedcentral.com)
  • Drug development companies are actively seeking to patent resveratrol-like molecules to create pharmaceuticals that would prevent and treat a wide range of age-related diseases, including diabetes, heart disease, cancer, and even Alzheimer's. (lifeextension.com)
  • MAIN OUTCOME MEASURES: LMS-based continuous reference percentiles for serum phosphate, plasma intact fibroblast growth factor 23 (iFGF23), and its cofactor soluble Klotho (sKlotho), tubular maximum phosphate reabsorption per glomerular filtration rate (TmP/GFR), fractional tubular reabsorption of phosphate (TRP), and urinary calcium/creatinine (Ca/Crea) and phosphate/creatinine (Pi/Crea) ratios. (bvsalud.org)
  • Compared to fed animals, fasted mice exhibited higher ß-hydroxybutyrate and FGF23 serum levels (based on assays either detecting C-terminal or intact, biologically active FGF23 only), cardiac, pancreatic, and thymic Fgf23 and renal Cyp24a1 expression, and lower 1,25(OH)2 D3 serum concentration as well as renal Slc34a1 and αKlotho (Kl) expression. (bvsalud.org)
  • Induced EndoMT in PAECs by inflammatory cytokines IL-1β, tumor necrosis factor α, and transforming growth factor β led to actin cytoskeleton reorganization and the development of a mesenchymal morphology. (surrey.ac.uk)
  • In addition, other studies demonstrated that AngII activated platelet-derived growth factor-A (PDGF-A), a novel contributor to cardiac remodelling, to result in atrial fibrosis in pressure-overloaded mouse model [ 13 ] . (medsci.org)
  • Fibroblast growth factor 23 (FGF23) is a peptide hormone mainly synthetized in the bone, regulating phosphate balance by blocking renal tubular phosphate reabsorption and inhibiting the synthesis of 1,25-dihydroxyvitamin D [ 1 ]. (biomedcentral.com)
  • It is generally believed that the early stages of hypertrophy can occur as a compensatory response to conditions such as chronic hypertension or valvular insufficiency. (europeanpharmaceuticalreview.com)
  • This provides a window of opportunity to slow or even reverse the progression of cardiac remodeling in these patients displaying the early stages of the disease. (adinstruments.com)
  • Min explains that during the early stages of cardiac hypertrophy, the changes in ventricular pressure and volume cause the PV Loop data to take on a distinctive shape. (adinstruments.com)
  • With time elapsing, the occurrence of cardiac hypertrophy can be divided into three stages: hypertrophy of the early, hypertrophy of the compensatory and the final decompensatory. (researchsquare.com)
  • These findings indicate that CS exposure worsens the progression of cardiac remodeling post-MI in male sex in a significant manner compared to female sex at least at early stages. (biomedcentral.com)
  • GATA4-targeted compounds 3i-1000 and 3i-1103 were identified as differential modulators of atrial and ventricular gene expression. (biomedcentral.com)
  • In this line, reporter gene assays with combinatorial treatment of 3i-1000 and the BET bromodomain inhibitor (+)-JQ1 demonstrated the cooperative role of GATA4 and BRD4 in the modulation of chamber-specific cardiac gene expression. (biomedcentral.com)
  • Using a variety of techniques including animal models of ventricular hypertrophy, gene knockouts, and hemodynamic analyses - Min and collegues have successfully identified some key proteins involved in the development of cardiac hypertrophy as well as potential drug targets and therapies for treating the disease 3,4,5 . (adinstruments.com)
  • theβ-myosin heavy chain(β-MHC)and atrial natriuretic factor (ANF), which are recognized as a marker of cardiac hypertrophy, were determined by Real-time quantitative PCR (qRT-PCR), then another gene phospholipase C (PLC), inositol triphosphate (IP 3 ), which associated with RAS were determined by Western blot(WB). (researchsquare.com)
  • A number sign (#) is used with this entry because of evidence that histiocytosis and lymphadenopathy with or without cutaneous, cardiac, and/or endocrine features, joint contractures, and/or deafness (histiocytosis-lymphadenopathy plus syndrome) is caused by homozygous or compound heterozygous mutation in the SLC29A3 gene (612373) on chromosome 10q22. (findzebra.com)
  • This study aimed to investigate the possible effect of TMZ on cardiac fibrosis exerted via the inhibition of NOX2-mediated EndMT. (dovepress.com)
  • Thus this research revealed the system by which avoided cardiac fibrosis after MI through a reduction in MCP-1 manifestation and an inhibition TEI-6720 TGF-β1 pathway and indicated puerarin is actually a potential agent in attenuating MI-induced cardiac fibrosis. (hiv-proteases.com)
  • Our data suggest that CKD reduces DMP1 expression, whereas its restoration represents a potential therapeutic approach to lower FGF23 and improve bone and cardiac health in CKD. (tamu.edu)
  • CONTEXT: The assessment of phosphate homeostasis in children is challenging due the marked changes in laboratory parameters during growth and development, and the lack of adequate reference values. (bvsalud.org)
  • Activity and outflow of renin--angiotensin--aldosterone system (RAAS) and ANS are enormously elevated in HF in order to maintain circulatory homeostasis and cardiac output [6,7]. (docksci.com)
  • However, a persistent mismatch between intrinsic compensatory capacity and increased workload will eventually induce further functional deterioration and alteration in ventricular geometry (ventricular remodeling). (centerforpediatricresearch.org)
  • Camelliti P, Borg TK, Kohl P. Structural and functional characterisation of cardiac fibroblasts. (pitt.edu)
  • Females did not display a significant structural and/or functional alteration within 7 days of cardiac remodeling post-MI upon CS exposure. (biomedcentral.com)
  • Understanding their mechanisms may lead to the development of microRNA cocktails that can potentially be used in regenerative cardiology. (archivesofmedicalscience.com)
  • Herren T., Gerber P. A., Duru F. Arrhythmogenic right ventricular cardiomyopathy /dysplasia: a not so rare «disease of the desmosome» with multiple clinical presentations // Clin. (vitapol.com.ua)
  • Today, 5-HT2B agonism is considered a toxicity signal precluding further clinical development of a compound. (wikipedia.org)
  • A better understanding of the pharmacological role of curcumin on diabetes and DCM can provide clinical implications for the intervention of the onset and development of diabetes and DCM. (frontiersin.org)
  • The discovery that mutations in sarcomere protein genes cause HCM has enabled the development of mouse models that recapitulate clinical manifestations of disease. (rupress.org)
  • Expression levels of RCAN homologs are responsive to external stressors such as reactive oxygen species, Ca 2+ , amyloid β, and hormonal changes and upregulated in pathological conditions, including Alzheimer's disease, cardiac hypertrophy, diabetes, and degenerative neuropathy. (molcells.org)
  • The development of new therapeutic tools for the treatment of this condition has in many cases been hampered by the lack of biologically relevant experimental models on which new treatments can be tested. (europeanpharmaceuticalreview.com)
  • These developments suggest that besides significant contributions to DS pathologies and calcineurin regulation, RCAN is an important participant across physiological systems, suggesting it as a favorable therapeutic target. (molcells.org)
  • For this purpose we developed a mouse model to investigate whether puerarin is a potential therapeutic compound for cardiac fibrosis induced by MI. (hiv-proteases.com)
  • ventricular and adrenergic Suppl: knowledge. (hone.world)
  • A cardiac fibrosis model was established in Sprague-Dawley rats through a subcutaneous injection of isoproterenol (ISO, 5 mg/kg/d). (dovepress.com)
  • The aim of this study was to evaluate the effect of 12 weeks aerobic training and oral green tea extract on cardiac caspase-3 expression in aged male rats. (ac.ir)