Fig. 1.

Schematic diagram of the pathophysiology of different cell phenotypes and representative pathways involved in infarct hearts (created with BioRender.com). After myocardial infarction, various cell signaling pathways are activated. Oxidative stress and the death of tissue, particularly apoptotic and necrotic cardiomyocytes, trigger the inflammatory response. Immunocytes infiltrate the infarct area and release inflammatory factors. Meanwhile, cardiac fibroblasts transform into cardiac myofibroblasts and secrete extracellular matrix, and endothelial cells migrate, proliferate and form a network of blood vessels to promote the cardiac repair. However, pathological hypertrophy of the myocardium affected by inflammation, coupled with reactive fibrosis, would eventually lead to cardiac remodeling and heart failure. MAPK, mitogen-activated protein kinase; Hippo/YAP, Hippo/Yes-associated protein; RhoA/ROCK, Ras homolog family member A/Rho associated coiled-coil containing protein kinase; Nrf2/HO-1, nuclear factor erythroid derived 2-related factor 2/heme oxygenase-1; TLR4/MyD88/NF-κB Toll-like receptor 4/MyD88/nuclear factor-κB; NLRP3/caspase-1, the nucleotide-binding domain, leucine-rich-repeat family, pyrin-domain-containing 3/caspase-1; TGF-β/SMADs, transforming growth factor-β/SMADs; Wnt/β-catenin, Wingless/β-catenin; PI3K/Akt, phosphoinositide-3 kinase/protein kinase B; EndoMT. endothelial-to-mesenchymal transition