Key result
Notch, Wnt, and PI3K pathways drive post-MI endothelial activation and reparative angiogenesis.
A deeper mechanistic understanding of post-infarction angiogenesis identifies promising epigenetic and molecular targets for future cardiac repair therapies.
Myocardial infarction (MI) causes massive loss of cardiac myocytes and injury to the coronary microcirculation, overwhelming the limited capacity of cardiac regeneration. Cardiac repair after MI is finely organized by complex series of procedures involving a robust angiogenic response that begins in the peri-infarcted border area of the infarcted heart, concluding with fibroblast proliferation and scar formation. Efficient neovascularization after MI limits hypertrophied myocytes and scar extent by the reduction in collagen deposition and sustains the improvement in cardiac function. Compelling evidence from animal models and classical in vitro angiogenic approaches demonstrate that a plethora of well-orchestrated signaling pathways involving Notch, Wnt, PI3K, and the modulation of intracellular Ca2+ concentration through ion channels, regulate angiogenesis from existing endothelial cells (ECs) and endothelial progenitor cells (EPCs) in the infarcted heart. Moreover, cardiac repair after MI involves cell-to-cell communication by paracrine/autocrine signals, mainly through the delivery of extracellular vesicles hosting pro-angiogenic proteins and non-coding RNAs, as microRNAs (miRNAs). This review highlights some general insights into signaling pathways activated under MI, focusing on the role of Ca2+ influx, Notch activated pathway, and miRNAs in EC activation and angiogenesis after MI.
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Martín-Bórnez et al. (2023) conducted a review in Myocardial Infarction. Signaling pathways and miRNAs regulating reparative angiogenesis was evaluated. Signaling pathways involving Notch, Wnt, PI3K, along with miRNAs and calcium influx, critically regulate endothelial cell activation and reparative angiogenesis following myocardial infarction.
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