ArticleThe Journal of clinical investigation1997
Changes in gene expression in the intact human heart. Downregulation of alpha-myosin heavy chain in hypertrophied, failing ventricular myocardium.
Article in The Journal of clinical investigation, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 168 papers.
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Who cites it
168 citing papers in PubMed, 502 citations in OpenAlex.
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- A gene regulatory element modulates myosin expression and controls cardiomyocyte response to stress.Genome research · 2025Article
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- Rare DCM associated variants in pre-miR-208a disrupt miRNA maturation and function.Human molecular genetics · 2025Article
- Cardiorenal Syndrome in Right Heart Failure Due to Pulmonary Arterial Hypertension-The Right Ventricle as a Therapeutic Target to Improve Renal Function.Cardiovascular drugs and therapy · 2025Review
- Identification of key genes for heart failure in dilated cardiomyopathy in different populations.Frontiers in genetics · 2025Article
- Analysis of age-related changes in the left ventricular myocardium with multiphoton microscopy.Biomedical optics express · 2024Article
- Zonisamide attenuates pressure overload-induced myocardial hypertrophy in mice through proteasome inhibition.Acta pharmacologica Sinica · 2024Article
- The Pathobiology of Myocardial Recovery and Remission: From Animal Models to Clinical Observations in Heart Failure Patients.Methodist DeBakey cardiovascular journal · 2024Review
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- Proteomic profiling of sudden cardiac death with acquired cardiac hypertrophy.International journal of legal medicine · 2023Article
- Functional and molecular determinants of right ventricular response to severe pulmonary hypertension in a large animal model.American journal of physiology. Heart and circulatory physiology · 2023Article
- Altered coronary artery function, arteriogenesis and endothelial YAP signaling in postnatal hypertrophic cardiomyopathy.Frontiers in physiology · 2023Article
- Human engineered cardiac tissue model of hypertrophic cardiomyopathy recapitulates key hallmarks of the disease and the effect of chronic mavacamten treatment.Frontiers in bioengineering and biotechnology · 2023Article
- Myosins and MyomiR Network in Patients with Obstructive Hypertrophic Cardiomyopathy.Biomedicines · 2022Article
- Normalization strategy for selection of reference genes for RT-qPCR analysis in left ventricles of failing human hearts.BMC cardiovascular disorders · 2022Article
- Loss of cardiac myosin light chain kinase contributes to contractile dysfunction in right ventricular pressure overload.Physiological reports · 2022Article
108 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 1 country.
Funding
Abstract
Using quantitative RT-PCR in RNA from right ventricular (RV) endomyocardial biopsies from intact nonfailing hearts, and subjects with moderate RV failure from primary pulmonary hypertension (PPH) or idiopathic dilated cardiomyopathy (IDC), we measured expression of genes involved in regulation of contractility or hypertrophy. Gene expression was also assessed in LV (left ventricular) and RV free wall and RV endomyocardium of hearts from end-stage IDC subjects undergoing heart transplantation or from nonfailing donors. In intact failing hearts, downregulation of beta1-receptor mRNA and protein, upregulation of atrial natriuretic peptide mRNA expression, and increased myocyte diameter indicated similar degrees of failure and hypertrophy in the IDC and PPH phenotypes. The only molecular phenotypic difference between PPH and IDC RVs was upregulation of beta2-receptor gene expression in PPH but not IDC. The major new findings were that (a) both nonfailing intact and explanted human ventricular myocardium expressed substantial amounts of alpha-myosin heavy chain mRNA (alpha-MHC, 23-34% of total), and (b) in heart failure alpha-MHC was downregulated (by 67-84%) and beta-MHC gene expression was upregulated. We conclude that at the mRNA level nonfailing human heart expresses substantial alpha-MHC. In myocardial failure this alteration in gene expression of MHC isoforms, if translated into protein expression, would decrease myosin ATPase enzyme velocity and slow speed of contraction.
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