• 2003). The aim of this study is to investigate the cellular mechanism by which UII results in ventricular hypertrophy. (bmj.com)
  • Cardiac hypertrophy is a fundamental response to an increased workload on the heart characterized by cardiac myocyte (CM) growth and left ventricular (LV) wall thickening. (dissertation.com)
  • These changes in turn can lead to the development of left ventricular hypertrophy (LVH), coronary artery disease (CAD), various conduction system diseases, and systolic and diastolic dysfunction of the myocardium, complications that manifest clinically as angina or myocardial infarction, cardiac arrhythmias (especially atrial fibrillation), and congestive heart failure (CHF). (medscape.com)
  • Two-dimensional echocardiogram (parasternal long axis view) from a 70-year-old woman showing concentric left ventricular hypertrophy and left atrial enlargement. (medscape.com)
  • Gross specimen of the heart with concentric left ventricular hypertrophy. (medscape.com)
  • Obesity has been linked to hypertension and left ventricular hypertrophy (LVH) in various epidemiologic studies, with as many as 50% of obese patients having some degree of hypertension and as many as 60-70% of patients with hypertension being obese. (medscape.com)
  • Unbiased ventricular microRNA (miRNA) arrays, mRNA sequencing, and lipid metabolism studies revealed dysregulation of cardiac hypertrophy, fibrosis, myocardial contractility, fatty acid transport/oxidation (FAO), and transforming growth factor-β signaling in the failing RV. (nih.gov)
  • Here, we describe the development of a TBX5/MYL2 lineage tracing reporter system that allows for the identification of FHF- progenitors and their descendants including left ventricular cardiomyocytes. (stanford.edu)
  • We compared this data with existing murine and 3D cardiac organoid scRNA-seq data and confirmed the dominance of left ventricular cardiomyocytes (>90%) in our hiPSC-derived progeny. (stanford.edu)
  • Furthermore, we conduct a cross-species prediction of cardiomyocyte subtypes from in vitro-derived human induced pluripotent stem cells and unexpectedly uncover a predominance of left ventricular (LV) identity that we confirmed by an LV-specific TBX5 lineage tracing system. (stanford.edu)
  • Oleanolic acid and ursolic acid induce hypertrophy in neonatal rat ventricular cardiomyocytes. (icbcongress.com)
  • Hypertrophic cardiomyopathy (HCM) is defined by ventricular hypertrophy. (cdc.gov)
  • Cerium oxide nanoparticle s attenuate monocrotaline induced right ventricular hypertrophy following pulmonary arterial hypertension. (cdc.gov)
  • Herein, we investigate whether CeO2 nanoparticle administration can diminish right ventricular (RV) hypertrophy following four weeks of monocrotaline (MCT)-induced pulmonary arterial hypertension (PAH). (cdc.gov)
  • Paralleling these changes in cardiac function, CeO2 nanoparticle treatment also diminished MCT-induced increases in right ventricular (RV) cardiomyocyte cross sectional area, ß-myosin heavy chain, fibronectin expression, protein nitrosylation, protein carbonylation and cardiac superoxide levels. (cdc.gov)
  • We analyzed standard reference RNA samples and RNA samples obtained from human induced pluripotent stem cell derived cardiomyocytes (hiPSC-CMs). (biomedcentral.com)
  • A study by Hashem et al using induced pluripotent stem cell-derived cardiomyocytes indicated that LAMP2 protein deficiency in Danon disease results in autophagic flux impairment, which in turn causes excessive oxidative stress and, subsequently, cardiomyocyte apoptosis. (medscape.com)
  • Isoproterenol infusion in control mice promoted overt cardiac hypertrophy and dysfunction (reduced ejection fraction, increased end systolic volume, increased cardiac weight index, increased cardiomyocyte area, increased fibrosis, and up-regulation of myocyte fetal genes and hypertrophy-associated microRNAs). (whiterose.ac.uk)
  • Through analyses of hypertrophic cardiomyocyte growth, fibrosis and cardiac function, delphinidin was demonstrated to confer resistance to aging- and transverse aortic constriction (TAC)-induced cardiac hypertrophy in vivo and attenuate Ang II-induced cardiomyocyte hypertrophy in vitro by significantly suppressing hypertrophic growth and the deposition of fibrosis. (nih.gov)
  • In summary, this present study would probe the influences of AREG on cardiac hypertrophy and fibrosis, and quest whether AREG regulates cardiac hypertrophy through affecting oxidative stress and apoptosis. (beds.ac.uk)
  • This cardiomyopathy may be due to either organ-based damage, such as fibrosis, or to direct damage to cardiomyocytes. (diabetesjournals.org)
  • In vitro mechanistic studies determined that cardiac fibroblasts responded to damaged myocardium by secreting several paracrine factors known to induce cardiomyocyte hypertrophy, including IL-6, whose secretion was dependent upon p38α activity. (whiterose.ac.uk)
  • In vitro , recombinant agrin promotes the division of cardiomyocytes that are derived from mouse and human induced pluripotent stem cells through a mechanism that involves the disassembly of the dystrophin-glycoprotein complex, and Yap- and ERK-mediated signalling. (nature.com)
  • This resulted in extreme cardiomyocyte proliferation and hypertrophy - excessive growth of the individual cardiomyocytes - leading to a giant heart (cardiomegaly) that left little room for blood to enter. (eurekalert.org)
  • To address these hypotheses, we examined contractility, Ca 2+ handling, and ROS levels in individual cardiomyocytes isolated from control hearts, diabetic OVE26 hearts, and diabetic hearts overexpressing antioxidant protein metallothionein (MT). Our data showed that diabetic myocytes exhibited significantly reduced peak shortening, prolonged duration of shortening/relengthening, and decreased maximal velocities of shortening/relengthening as well as slowed intracellular Ca 2+ decay compared with control myocytes. (diabetesjournals.org)
  • Adult cardiomyocytes in mice primarily express alpha-myosin heavy chain (alpha-MHC, also known as Myh6), whereas embryonic cardiomyocytes express beta-MHC (also known as Myh7). (ca.gov)
  • Eighteen-month-old mice were administered delphinidin to investigate the effect of delphinidin on aging-related cardiac hypertrophy. (nih.gov)
  • The team then created mice in which the gene for ERBB2 was knocked out only in cardiomyocytes. (eurekalert.org)
  • We report that deletion of PPARγ in cardiomyocytes leads to biventricular systolic dysfunction and intramyocellular lipid accumulation in mice. (nih.gov)
  • Here we show that changes in the composition of the extracellular matrix during this week can affect cardiomyocyte growth and differentiation in mice. (nature.com)
  • In vivo , a single administration of agrin promotes cardiac regeneration in adult mice after myocardial infarction, although the degree of cardiomyocyte proliferation observed in this model suggests that there are additional therapeutic mechanisms. (nature.com)
  • Moreover, Trpc1(-)(/)(-) mice fail to manifest evidence of maladaptive cardiac hypertrophy and maintain preserved cardiac function when subjected to hemodynamic stress and neurohormonal excess. (duke.edu)
  • Here, we show that treatment of cultured neonatal rat cardiomyocytes with the hypertrophic agonist norepinephrine promotes mitochondrial fission (characterized by a decrease in mitochondrial mean volume and an increase in the relative number of mitochondria per cell ) and a decrease in mitochondrial function. (bvsalud.org)
  • We have shown that kinase inhibitor-induced cardiac injury arises as a result of both on- and off- target effects, may of which affect cardiomyocyte metabolism. (unc.edu)
  • Recent studies suggest that cardiac fibroblast-specific p38α MAPK contributes to the development of cardiac hypertrophy, but the underlying mechanism is unknown. (whiterose.ac.uk)
  • Using alpha-adrenergic receptor (αAR) stimulation as a model of Gq-mediated hypertrophy, we found that C674S expression decreased both CM growth and MAPK activation. (dissertation.com)
  • These findings led us to the conclusion that redox-activation of SERCA via reversible modification of C674 is critical for the complete transduction of hypertrophic stimuli to MAPK signaling and CM hypertrophy. (dissertation.com)
  • Res effectively suppress the cardiomyocytes hypertrophy and apoptosis induced by ISO, characterized by the reduction of the myocardial cell surface area, the ANP gene expression, the LDH and MDA leakage amount and the rate of cell apoptosis, while decrease of the protein expression of GRP78, GRP94 and CHOP, and reverse the expression of Bcl-2 and Bax. (karger.com)
  • The purpose of this research was to explore the role of AREG on cardiomyocytes apoptosis of hypertrophic cardiomyopathy. (beds.ac.uk)
  • Loss of cardiomyocytes is a major cause of heart failure, and while the adult heart has a limited capacity for cardiomyogenesis, little is known about what regulates this ability or whether it can be effectively harnessed. (researchgate.net)
  • Activation of the α1A protects against cardiomyocyte death and increases contractility in the failing heart, though the mechanisms underlying these adaptive effects are incompletely understood. (unc.edu)
  • Figure 1: Identification of agrin in a screen for mouse cardiac ECM-mediated cardiomyocyte proliferation. (nature.com)
  • Figure 4: Agrin promotes cardiomyocyte proliferation through Dag1, ERK and Yap signalling. (nature.com)
  • Cardiac stress triggers adult hearts to undergo hypertrophy and a shift from alpha-MHC to fetal beta-MHC expression. (ca.gov)
  • Next, the team reactivated the ERBB2 protein in adult mouse heart cells, in which cardiomyocytes normally no longer divide. (eurekalert.org)
  • The question then became: If one could activate ERBB2 for just a short period in an adult heart following a heart attack, might it be possible to get the positive results, i.e., cardiac cell renewal, without such negative ones as hypertrophy and scarring? (eurekalert.org)
  • Investigation of the regenerative process through live imaging and molecular studies revealed how this happens: The cardiomyocytes "dedifferentiate" - that is, they revert to an earlier form, something between an embryonic and an adult cell, which can then divide and differentiate into new heart cells. (eurekalert.org)
  • The adult mammalian heart is non-regenerative owing to the post-mitotic nature of cardiomyocytes. (nature.com)
  • METHODS AND RESULTS: Here, we used whole cell patch clamp of adult cardiomyocytes to show upregulation of a nonselective cation current reminiscent of TRPC channels subjected to pressure overload. (duke.edu)
  • Failing RV cardiomyocytes exhibited mitochondrial disarray and increased intramyocellular lipids (lipotoxicity) in the SuHx heart, which was prevented by pioglitazone. (nih.gov)
  • However, the broader phenotype includes abnormal cardiomyocyte orientation (disarray), myocardial ischaemia and electrical abnormalities, which seem to manifest before overt hypertrophy. (cdc.gov)
  • 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)
  • This inactivation has been identified as a possible contributing factor to the onset of cardiomyocyte binucleation during the neonatal period. (wikipedia.org)
  • Consistently, pre-miR-197 and pre-miR-146b repressed genes that drive FAO ( Cpt1b and Fabp4 ) in primary cardiomyocytes. (nih.gov)
  • RATIONALE: Cardiac muscle adapts to increase workload by altering cardiomyocyte size and function resulting in cardiac hypertrophy. (duke.edu)
  • Pathological cardiac hypertrophy begins with an adaptive response to increased workload. (beds.ac.uk)
  • CONCLUSIONS: From these studies, we suggest that TRPC1 channels are critical for the adaptation to biomechanical stress and TRPC dysregulation leads to maladaptive cardiac hypertrophy and failure. (duke.edu)
  • This study was undertaken to investigate whether Res can protect the heart suffering from hypertrophy injuries induced by isoproterenol (ISO), and whether the protective effect is mediated by endoplasmic reticulum (ER) stress. (karger.com)
  • In cardiomyocytes, CaMKII phosphorylation of HDAC4 results in hypertrophic growth, which can be blocked by a signal-resistant HDAC4 mutant. (jci.org)
  • To study the role of ERK1/2, P38 and CaMKII signalling in the UII-induced hypertrophy, cultured ARVMs were treated with either 5µM of ERK1/2 inhibitor (PD 184352), 10 µM of P38 inhibitor (SB 202190) or 5 µM CaMKII (KN-93) for 30 min prior to stimulation with UII (200 nM). (bmj.com)
  • Mitochondrial fission is required for cardiomyocyte hypertrophy mediated by a Ca2+-calcineurin signaling pathway. (bvsalud.org)
  • Cardiomyocyte hypertrophy has been associated with diminished mitochondrial metabolism . (bvsalud.org)
  • The relationship between mitochondrial dynamics and cardiomyocyte hypertrophy is still poorly understood. (bvsalud.org)
  • Dominant-negative Drp1 (K38A) not only prevented mitochondrial fission , it also blocked hypertrophic growth of cardiomyocytes in response to norepinephrine . (bvsalud.org)
  • Collectively, these results demonstrate the importance of mitochondrial dynamics in the development of cardiomyocyte hypertrophy and metabolic remodeling . (bvsalud.org)
  • Cardiac function was assessed by pressure-volume conductance catheter analysis and was evaluated for cardiac hypertrophy at tissue, cellular, and molecular levels. (whiterose.ac.uk)
  • Classical and immunohistologic analyses indicated only a slight cardiomyocyte hypertrophy without myocarditis per the Dallas criteria ( 8 ). (cdc.gov)
  • Background: Physiological cardiac hypertrophy occurs commonly in response to exercise and can protect against pathological stress. (researchgate.net)
  • In conclusion, cardiac fibroblast p38α contributes to cardiomyocyte hypertrophy and cardiac dysfunction, potentially via a mechanism involving paracrine fibroblast-to-myocyte IL-6 signaling. (whiterose.ac.uk)
  • Hypertrophy was estimated by measuring the cell surface area and the atrial natriuretic peptide (ANP) gene expression. (karger.com)
  • Cardiac hypertrophy and failure are characterized by transcriptional reprogramming of gene expression. (ca.gov)
  • Our studies show that Brg1 maintains cardiomyocytes in an embryonic state, and demonstrate an epigenetic mechanism by which three classes of chromatin-modifying factors-Brg1, HDAC and PARP-cooperate to control developmental and pathological gene expression. (ca.gov)
  • Our study used a novel fibroblast-specific, tamoxifen-inducible p38α knockout (KO) mouse line to characterize the role of fibroblast p38α in modulating cardiac hypertrophy, and we elucidated the mechanism. (whiterose.ac.uk)
  • After AREG downregulation, the increases of Ang II induced cardiac weight and cardiomyocytes area were inhibited. (beds.ac.uk)
  • The conclusion was that cardiomyocytes lacking ERBB2 do not divide, even in the presence of NRG1. (eurekalert.org)
  • 2002). UII has been shown to be involved the development of pathological cardiac hypertrophy (Tzanidis et al. (bmj.com)
  • During the pathological development of cardiovascular diseases, cardiac hypertrophy plays a critical role. (karger.com)
  • Reactive oxygen species (ROS) play a pivotal role in the development of pathological cardiac hypertrophy. (nih.gov)
  • The mechanisms underlying the development of cardiac hypertrophy are yet not well understood. (mdpi.com)
  • G protein-coupled receptor signaling is known to govern the hypertrophic response through the regulation of ion channel activity and downstream signaling in failing cardiomyocytes. (duke.edu)
  • OBJECTIVE: Transient receptor potential canonical (TRPC) channels are G protein-coupled receptor operated channels previously implicated in cardiac hypertrophy. (duke.edu)
  • image: Two neonatal cardiomyocytes (stained red) undergoing cell division after treatment with NRG1 are shown. (eurekalert.org)
  • Upon myocardial infarction (MI) immune system becomes activated by extensive necrosis of cardiomyocytes and release of damage-associated molecular patterns [ 16 ]. (springer.com)