ArticleInternational journal of molecular sciences2024
Extracellular PKM2 Preserves Cardiomyocytes and Reduces Cardiac Fibrosis During Myocardial Infarction.
Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- Rewiring the scar: translational advances in cardiac fibrosis.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025Review
- Review
- Pyruvate kinase splice variants in fibroblasts influence cardiac remodeling after myocardial infarction in male mice.Journal of molecular and cellular cardiology · 2025Article
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Authors and funding
10 authors.
Funding
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Abstract
Substantial loss of cardiomyocytes during heart attacks and onset of other cardiovascular diseases is a major cause of mortality. Preservation of cardiomyocytes during cardiac injury would be the most effective strategy to manage these diseases in clinic. However, there is no effective treatment strategy that is able to prevent cardiomyocyte loss. We demonstrate here that the systemic administration of a recombinant PKM2 mutant (G415R) preserves cardiomyocytes and reduces cardiac fibrosis during myocardial infarction. G415R preserves cardiomyocytes by protecting the cardiomyocytes from dying and by promoting cardiomyocyte proliferation. Preservation of cardiomyocytes by extracellular PKM2 (EcPKM2) reduces cardiac fibrosis because of the decreased activation of cardiac fibroblasts. Our experiments show that EcPKM2 (G415R) exerts its action by interacting with integrin a
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