ArticleThe Journal of clinical investigation1987
Myosin heavy chain messenger RNA and protein isoform transitions during cardiac hypertrophy. Interaction between hemodynamic and thyroid hormone-induced signals.
Article in The Journal of clinical investigation, 1987. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 103 papers.
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Who cites it
103 citing papers in PubMed.
- Article
- Transcriptional regulation in heart development, disease and regeneration: reassessing the fetal gene hypothesis.Nature reviews. Cardiology · 2026Review
- Disease-modifying effects of iron deficiency in mouse models of chronic renal failure.Blood red cells & iron · 2025Article
- Long non-coding RNAs in cardiac hypertrophy and heart failure: functions, mechanisms and clinical prospects.Nature reviews. Cardiology · 2024Review
- Thrombospondin-1 Drives Cardiac Remodeling in Chronic Kidney Disease.JACC. Basic to translational science · 2024Article
- Article
- Drug Development and the Use of Induced Pluripotent Stem Cell-Derived Cardiomyocytes for Disease Modeling and Drug Toxicity Screening.International journal of molecular sciences · 2020Review
- miR-206 enforces a slow muscle phenotype.Journal of cell science · 2020Article
- Sex-Based Mhrt Methylation Chromatinizes MeCP2 in the Heart.iScience · 2019Article
- Modeling Human Cardiac Hypertrophy in Stem Cell-Derived Cardiomyocytes.Stem cell reports · 2018Article
- Molecular mechanisms of cardioprotective effects mediated by transplanted cardiac ckitOncotarget · 2018Article
- The cardioprotective effect of dexrazoxane (Cardioxane) is consistent with sequestration of poly(ADP-ribose) by self-assembly and not depletion of topoisomerase 2B.Ecancermedicalscience · 2018Article
- Novel large-particle FACS purification of adult ventricular myocytes reveals accumulation of myosin and actin disproportionate to cell size and proteome in normal post-weaning development.Journal of molecular and cellular cardiology · 2017Article
- Iron overload exacerbates age-associated cardiac hypertrophy in a mouse model of hemochromatosis.Scientific reports · 2017Article
- Complete Characterization of Cardiac Myosin Heavy Chain (223 kDa) Enabled by Size-Exclusion Chromatography and Middle-Down Mass Spectrometry.Analytical chemistry · 2017Article
- Muscle Stem Cell and Physical Activity: What Point is the Debate at?Open medicine (Warsaw, Poland) · 2017Article
- Cinaciguat prevents the development of pathologic hypertrophy in a rat model of left ventricular pressure overload.Scientific reports · 2016Article
- A post-MI power struggle: adaptations in cardiac power occur at the sarcomere level alongside MyBP-C and RLC phosphorylation.American journal of physiology. Heart and circulatory physiology · 2016Article
- Abrogation of Nrf2 impairs antioxidant signaling and promotes atrial hypertrophy in response to high-intensity exercise stress.Journal of translational medicine · 2016Article
- Activation of Cardiac Fibroblast Growth Factor Receptor 4 Causes Left Ventricular Hypertrophy.Cell metabolism · 2015Article
43 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Expression of the cardiac myosin isozymes is regulated during development, by hormonal stimuli and hemodynamic load. In this study, the levels of expression of the two isoforms (alpha and beta) of myosin heavy chain (MHC) during cardiac hypertrophy were investigated at the messenger RNA (mRNA) and protein levels. In normal control and sham-operated rats, the alpha-MHC mRNA predominated in the ventricular myocardium. In response to aortic coarctation, there was a rapid induction of the beta-MHC mRNA followed by the appearance of comparable levels of the beta-MHC protein in parallel to an increase in the left ventricular weight. Administration of thyroxine to coarctated animals caused a rapid deinduction of beta-MHC and induction of alpha-MHC, both at the mRNA and protein levels, despite progression of left ventricular hypertrophy. These results suggest that the MHC isozyme transition during hemodynamic overload is mainly regulated by pretranslational mechanisms, and that a complex interplay exists between hemodynamic and hormonal stimuli in MHC gene expression.
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