ArticleJournal of the American Heart Association2019
Expression of Normally Repressed Myosin Heavy Chain 7b in the Mammalian Heart Induces Dilated Cardiomyopathy.
Article in Journal of the American Heart Association, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 29 citations in OpenAlex.
- An integrative single-nucleus multiomic atlas of the human left ventricle identifies gene regulatory network dynamics across cardiac development, aging, and disease.Genome biology · 2026Article
- Peptidyl-tRNA hydrolase 2 is a negative regulator of peripartum cardiomyopathy with heart failure in female mice.Nature communications · 2025Article
- Myocardial transcriptomic and proteomic landscapes across the menopausal continuum in a murine model of chemically induced accelerated ovarian failure.Physiological genomics · 2025Article
- Transcriptomic Profiling of Zebrafish Mutant forInternational journal of molecular sciences · 2025Article
- Transcriptomic Profiling of Human Myocardium at Sudden Death to Define Vulnerable Substrate for Lethal Arrhythmias.JACC. Clinical electrophysiology · 2025Article
- Postprandial cardiac hypertrophy is sustained by mechanics, epigenetic, and metabolic reprogramming in pythons.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- A Laing distal myopathy-associated proline substitution in the β-myosin rod perturbs myosin cross-bridging activity.The Journal of clinical investigation · 2024Article
- Low-intensity exercise training improves systolic function of heart during metastatic melanoma-induced cachexia in mice.Heliyon · 2024Article
- Dual roles of myocardial mitochondrial AKT on diabetic cardiomyopathy and whole body metabolism.Cardiovascular diabetology · 2023Article
- Post-ischemic cardioprotective potential of exogenous ubiquitin in myocardial remodeling late after ischemia/reperfusion injury.Life sciences · 2023Article
- Myosins and MyomiR Network in Patients with Obstructive Hypertrophic Cardiomyopathy.Biomedicines · 2022Article
- Cardiac sarcomere mechanics in health and disease.Biophysical reviews · 2021Review
- Untangling the Cooperative Role of Nuclear Receptors in Cardiovascular Physiology and Disease.International journal of molecular sciences · 2021Review
- Nonproductive Splicing Prevents Expression of MYH7b Protein in the Mammalian Heart.Journal of the American Heart Association · 2021Article
- MYH7B variants cause hypertrophic cardiomyopathy by activating the CaMK-signaling pathway.Science China. Life sciences · 2020Article
- Expression of Normally Repressed Myosin Heavy Chain 7b in the Mammalian Heart Induces Dilated Cardiomyopathy.Journal of the American Heart Association · 2019Article
- Myosin 7b is a regulatory long noncoding RNA (lncMYH7b) in the human heart.The Journal of biological chemistryArticle
Corrections and comments
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Authors and funding
9 authors at 1 institution in 2 countries.
Funding
Abstract
Background In mammals, muscle contraction is controlled by a family of 10 sarcomeric myosin motors. The expression of one of its members, MYH7b, is regulated by alternative splicing, and while the protein is restricted to specialized muscles such as extraocular muscles or muscle spindles, RNA that cannot encode protein is expressed in most skeletal muscles and in the heart. Remarkably, birds and snakes express MYH7b protein in both heart and skeletal muscles. This observation suggests that in the mammalian heart, the motor activity of MYH7b may only be needed during development since its expression is prevented in adult tissue, possibly because it could promote disease by unbalancing myocardial contractility. Methods and Results We have analyzed MYH7b null mice to determine the potential role of MYH7b during cardiac development and also generated transgenic mice with cardiac myocyte expression of MYH7b protein to measure its impact on cardiomyocyte function and contractility. We found that MYH7b null mice are born at expected Mendelian ratios and do not have a baseline cardiac phenotype as adults. In contrast, transgenic cardiac MYH7b protein expression induced early cardiac dilation in males with significantly increased left ventricular mass in both sexes. Cardiac dilation is progressive, leading to early cardiac dysfunction in males, but later dysfunction in females. Conclusions The data presented show that the expression of MYH7b protein in the mammalian heart has been inhibited during the evolution of mammals most likely to prevent the development of a severe cardiomyopathy that is sexually dimorphic.
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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.