ArticleThe Journal of clinical investigation1998
Myofibril degeneration caused by tropomodulin overexpression leads to dilated cardiomyopathy in juvenile mice.
Article in The Journal of clinical investigation, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
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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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Who cites it
63 citing papers in PubMed, 165 citations in OpenAlex.
- Cardiomyocyte-Specific Smad7 Protects the Pressure-Overloaded Heart, Inhibiting the Transforming Growth Factor-β Receptor 1/Smad2/3 Cascade.Journal of the American Heart Association · 2026Article
- Metrics of left ventricular active relaxation reflect proteomic myocardial remodelling and reverse remodelling.ESC heart failure · 2026Article
- Tropomodulin-Tropomyosin Interplay Modulates Interaction Between Cardiac Myosin and Thin Filaments.Biomolecules · 2025Article
- Review
- A human FLII gene variant alters sarcomeric actin thin filament length and predisposes to cardiomyopathy.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- The Mechanisms of Thin Filament Assembly and Length Regulation in Muscles.International journal of molecular sciences · 2022Review
- Dilated cardiomyopathy: a new insight into the rare but common cause of heart failure.Heart failure reviews · 2022Review
- SIRT1 activation and its effect on intercalated disc proteins as a way to reduce doxorubicin cardiotoxicity.Frontiers in pharmacology · 2022Review
- Novel insights into sarcomere regulatory systems control of cardiac thin filament activation.The Journal of general physiology · 2021Article
- Retrospective Study of Intercalated Disk Defects Associated with Dilated Cardiomyopathy, Atrial Thrombosis, and Heart Failure in BALB/c Mice Deficient in IL4 Receptor α.Comparative medicine · 2020Article
- Article
- Tropomodulin1 Expression Increases Upon Maturation in Dendritic Cells and Promotes Their Maturation and Immune Functions.Frontiers in immunology · 2020Article
- Quantitative proteomics reveals TMOD1-related proteins associated with water balance regulation.PloS one · 2019Article
- Actin-associated proteins and cardiomyopathy-the 'unknown' beyond troponin and tropomyosin.Biophysical reviews · 2018Review
- HSPB7 is indispensable for heart development by modulating actin filament assembly.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Overview of the Muscle Cytoskeleton.Comprehensive Physiology · 2017Review
- Relevance of mouse models of cardiac fibrosis and hypertrophy in cardiac research.Molecular and cellular biochemistry · 2017Review
- Quantitative Non-canonical Amino Acid Tagging (QuaNCAT) Proteomics Identifies Distinct Patterns of Protein Synthesis Rapidly Induced by Hypertrophic Agents in Cardiomyocytes, Revealing New Aspects of Metabolic Remodeling.Molecular & cellular proteomics : MCP · 2016Article
- Thin filament length in the cardiac sarcomere varies with sarcomere length but is independent of titin and nebulin.Journal of molecular and cellular cardiology · 2016Article
- Localization of the binding interface between leiomodin-2 and α-tropomyosin.Biochimica et biophysica acta · 2016Article
3 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
8 authors at 4 institutions in 1 country.
Funding
Abstract
Loss of myofibril organization is a common feature of chronic dilated and progressive cardiomyopathy. To study how the heart compensates for myofibril degeneration, transgenic mice were created that undergo progressive loss of myofibrils after birth. Myofibril degeneration was induced by overexpression of tropomodulin, a component of the thin filament complex which determines and maintains sarcomeric actin filament length. The tropomodulin cDNA was placed under control of the alpha-myosin heavy chain gene promoter to overexpress tropomodulin specifically in the myocardium. Offspring with the most severe phenotype showed cardiomyopathic changes between 2 and 4 wk after birth. Hearts from these mice present characteristics consistent with dilated cardiomyopathy and a failed hypertrophic response. Histological analysis showed widespread loss of myofibril organization. Confocal microscopy of isolated cardiomyocytes revealed intense tropomodulin immunoreactivity in transgenic mice together with abnormal coincidence of tropomodulin and alpha-actinin reactivity at Z discs. Contractile function was compromised severely as determined by echocardiographic analyses and isolated Langendorff heart preparations. This novel experimentally induced cardiomyopathy will be useful for understanding dilated cardiomyopathy and the effect of thin filament-based myofibril degeneration upon cardiac structure and function.
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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.