Key result
Targeting growth factor signaling pathways offers therapeutic potential to prevent post-MI remodeling and heart failure.
This literature review summarizes the molecular mechanisms of the reparative response in myocardial infarction and identifies growth factors, their receptors, and cellular signaling pathways as promising therapeutic targets to prevent post-infarct remodeling and chronic heart failure.
May guide post-MI therapeutic development; leaves open clinical efficacy pending prospective trials.
Post-infarction scar formation after myocardial infarction (MI) is a complex dynamic process involving stages of inflammation, proliferation, and scar maturation. Reparative processes in MI mainly occur during the proliferation stage, including angiogenesis, fibrogenesis, and cardiomyogenesis, the latter characterized by insufficient effectiveness for complete myocardial recovery after irreversible damage. The review summarizes current data on the molecular mechanisms of the reparative response in MI, which involves both resident myocardial cells and leukocytes, stem and progenitor cells recruited from the bloodstream. Growth factors, cytokines, and biologically active substances play an important role in the regulation of cellular processes occurring at the proliferation stage after MI. The local concentration of growth factors in the damaged myocardium, as well as the dynamics of their formation, determine the outcomes of ischemic myocardial damage associated with postinfarct remodeling and the likelihood of developing chronic heart failure. This allows us to consider growth factors, their receptors, and cellular signaling pathways as promising therapeutic targets to prevent adverse outcomes after MI.
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Cheburkin et al. (2026) conducted a review in Myocardial infarction. Growth factors, their receptors, and cellular signaling pathways was evaluated on Postinfarct remodeling and chronic heart failure. Growth factors, their receptors, and cellular signaling pathways regulate post-MI proliferation and represent promising therapeutic targets to prevent postinfarct remodeling and heart failure.
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