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Myocardial tissue repair refers to the complex biological processes involved in restoring the integrity and function of the heart muscle following injury, most commonly after a myocardial infarction (MI). In adult humans, the heart possesses a very limited intrinsic regenerative capacity, typically responding to damage through a wound-healing process that results in permanent, non-contractile fibrotic scarring rather than functional muscle replacement [PMID: 25023144]. This process involves an initial inflammatory phase, a proliferative phase characterized by fibroblast activation and angiogenesis, and a maturation phase where the extracellular matrix is remodeled [PMID: 24561462]. Therapeutic strategies in this field aim to shift the balance from scarring toward true regeneration by stimulating endogenous cardiomyocyte proliferation or utilizing exogenous cell-based and gene therapies [PMID: 30135558]. Key molecular pathways regulating this repair include the Hippo-YAP, Wnt, and Notch signaling pathways, as well as various growth factor cascades [PMID: 28249162]. Because Myocardial tissue repair describes a multi-faceted physiological outcome rather than a single protein, enzyme, or receptor, it is classified as a therapeutic goal or biological process rather than a discrete molecular drug target.
Stimulation of endogenous repair mechanisms, promotion of angiogenesis, and modulation of the inflammatory response to reduce fibrotic scarring and restore contractile function.
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