ReviewJournal of molecular and cellular cardiology2007
Factors controlling cardiac myosin-isoform shift during hypertrophy and heart failure.
Review in Journal of molecular and cellular cardiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 122 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
122 citing papers in PubMed, 222 citations in OpenAlex.
- Article
- Contrasting the genetic architecture of cardiac glutathione against other organs: unveiling a unique tissue-specific locus.Mammalian genome : official journal of the International Mammalian Genome Society · 2026Article
- Molecular Mediators of the Cardiac Benefits of Exercise.Circulation research · 2025Review
- Molecular Mechanisms of Type 2 Diabetes-Related Heart Disease and Therapeutic Insights.International journal of molecular sciences · 2025Review
- Chronic moderate‑intensity exercise can induce physiological hypertrophy in aged cardiomyocytes through autophagy, with minimal Yap/Taz involvement.Biomedical reports · 2025Article
- Gestational arsenite exposure alters maternal postpartum heart size and induces CaAmerican journal of physiology. Heart and circulatory physiology · 2025Article
- Transcriptomics, Proteomics and Bioinformatics in Atrial Fibrillation: A Descriptive Review.Bioengineering (Basel, Switzerland) · 2025Review
- Severe Phenotype of De Novo TSHR Activating Pathogenic Variants.Case reports in endocrinology · 2025Article
- Epac1 increases myosin regulatory light-chain phosphorylation, energetic cost of contraction, and susceptibility to heart failure.PloS one · 2025Article
- Sex-specific regulation of the cardiac transcriptome by the protein phosphatase 2A regulatory subunit B55α.npj metabolic health and disease · 2024Article
- Perinatal Inflammation Results in Sex-Dependent Cardiac Dysfunction.Journal of cardiovascular development and disease · 2024Article
- The splicing factor hnRNPL demonstrates conserved myocardial regulation across species and is altered in heart failure.FEBS letters · 2024Article
- UCP1-dependent brown adipose activation accelerates cardiac metabolic remodeling and reduces initial hypertrophic and fibrotic responses to pathological stress.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- Analysis of age-related changes in the left ventricular myocardium with multiphoton microscopy.Biomedical optics express · 2024Article
- Detecting differential transcript usage in complex diseases with SPIT.Cell reports methods · 2024Article
- Proteomic Profiling of SGLT-2 Inhibitor Canagliflozin in a Swine Model of Chronic Myocardial Ischemia.Biomedicines · 2024Article
- Hypoxia Attenuates Pressure Overload-Induced Heart Failure.Journal of the American Heart Association · 2024Article
- miR-29a activates expression of α-cardiac myosin heavy chain via β1 thyroid hormone receptor in neonatal rats.Archives of medical science : AMS · 2024Article
- Cardiometabolic Index is associated with heart failure: a cross-sectional study based on NHANES.Frontiers in medicine · 2024Article
- Sibjotang Protects against Cardiac Hypertrophy In Vitro and In Vivo.Life (Basel, Switzerland) · 2023Article
62 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Myosin is a molecular motor, which interacts with actin to convert the energy from ATP hydrolysis into mechanical work. In cardiac myocytes, two myosin isoforms are expressed and their relative distribution changes in different developmental and pathophysiologic conditions of the heart. It has been realized for a long time that a shift in myosin isoforms plays a major role in regulating myocardial contractile activity. With the recent evidence implicating that alteration in myosin isoform ratio may be eventually beneficial for the treatment of a stressed heart, a new interest has developed to find out ways of controlling the myosin isoform shift. This article reviews the published data describing the role of myosin isoforms in the heart and highlighting the importance of various factors shown to influence myosin isofrom shift during physiology and disease states of the heart.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.