TGFB1 and infarction: It inhibits post-infarction inflammatory responses through interactions with hyaluronic acid, stimulates the TGF-β signaling pathway, promotes fibroblast infiltration and proliferation, and ultimately enhances collagen deposition.139 In the late stage of IRI, CCL2 stimulates the transformation of CCR2+ macrophages into a reparative phenotype and releases TGF-β to promote fibrosis.141 When it comes to pro-repair CCR2- macrophages, Li et al. unveiled their ability to produce small extracellular vesicles (sEVs).