ArticleBasic research in cardiology2011
EH-myomesin splice isoform is a novel marker for dilated cardiomyopathy.
Article in Basic research in cardiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 58 citations in OpenAlex.
- Alternative Splicing in Mechanically Stretched Podocytes as a Model of Glomerular Hypertension.Journal of the American Society of Nephrology : JASN · 2025Article
- Human induced pluripotent stem cell-derived cardiomyocytes for disease modeling and drug discovery.Frontiers in bioengineering and biotechnology · 2025Review
- Proteomic and metabolomic analyses of the human adult myocardium reveal ventricle-specific regulation in end-stage cardiomyopathies.Communications biology · 2024Article
- Loss of Cardiac Splicing RegulatorJACC. Basic to translational science · 2024Article
- Cardiac maturation.Journal of molecular and cellular cardiology · 2024Review
- Myofilament-associated proteins with intrinsic disorder (MAPIDs) and their resolution by computational modeling.Quarterly reviews of biophysics · 2023Review
- Sarcomere maturation: function acquisition, molecular mechanism, and interplay with other organelles.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2022Review
- Fine-tuned KDM1A alternative splicing regulates human cardiomyogenesis through an enzymatic-independent mechanism.iScience · 2022Article
- The role of the M-band myomesin proteins in muscle integrity and cardiac disease.Journal of biomedical science · 2022Review
- Understanding the molecular basis of cardiomyopathy.American journal of physiology. Heart and circulatory physiology · 2022Review
- Splicing factor Srsf5 deletion disrupts alternative splicing and causes noncompaction of ventricular myocardium.iScience · 2021Article
- Knockout of MYOM1 in human cardiomyocytes leads to myocardial atrophy via impairing calcium homeostasis.Journal of cellular and molecular medicine · 2021Article
- Phosphoproteomic Analysis Reveals Downstream PKA Effectors of AKAP Cypher/ZASP in the Pathogenesis of Dilated Cardiomyopathy.Frontiers in cardiovascular medicine · 2021Article
- Identification ofDisease models & mechanisms · 2020Article
- The M-band: The underestimated part of the sarcomere.Biochimica et biophysica acta. Molecular cell research · 2020Review
- Deleting Full Length Titin Versus the Titin M-Band Region Leads to Differential Mechanosignaling and Cardiac Phenotypes.Circulation · 2019Article
- Myomesin is part of an integrity pathway that responds to sarcomere damage and disease.PloS one · 2019Article
- Alternative splicing in cardiomyopathy.Biophysical reviews · 2018Review
- Alternative splicing isoforms in health and disease.Pflugers Archiv : European journal of physiology · 2018Review
- Thick Filament Protein Network, Functions, and Disease Association.Comprehensive Physiology · 2018Review
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Authors and funding
12 authors at 6 institutions in 3 countries.
Funding
Abstract
The M-band is the prominent cytoskeletal structure that cross-links the myosin and titin filaments in the middle of the sarcomere. To investigate M-band alterations in heart disease, we analyzed the expression of its main components, proteins of the myomesin family, in mouse and human cardiomyopathy. Cardiac function was assessed by echocardiography and compared to the expression pattern of myomesins evaluated with RT-PCR, Western blot, and immunofluorescent analysis. Disease progression in transgenic mouse models for dilated cardiomyopathy (DCM) was accompanied by specific M-band alterations. The dominant splice isoform in the embryonic heart, EH-myomesin, was strongly up-regulated in the failing heart and correlated with a decrease in cardiac function (R = -0.86). In addition, we have analyzed the expressions of myomesins in human myocardial biopsies (N = 40) obtained from DCM patients, DCM patients supported by a left ventricular assist device (LVAD), hypertrophic cardiomyopathy (HCM) patients and controls. Quantitative RT-PCR revealed that the EH-myomesin isoform was up-regulated 41-fold (P < 0.001) in the DCM patients compared to control patients. In DCM hearts supported by a LVAD and HCM hearts, the EH-myomesin expression was comparable to controls. Immunofluorescent analyses indicate that EH-myomesin was enhanced in a cell-specific manner, leading to a higher heterogeneity of the myocytes' cytoskeleton through the myocardial wall. We suggest that the up-regulation of EH-myomesin denotes an adaptive remodeling of the sarcomere cytoskeleton in the dilated heart and might serve as a marker for DCM in mouse and human myocardium.
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