Fig. 1

Functions of the ASC secretome on the ischemic heart. Lots of trophic factors released by ASCs, such as VEGF, HGF, PGF, TGF-β, FGF-2, Ang-1, and Ang-2, IGF-1, and microvesicles, miR-31 and miR-126, benefit for proangiogenesis in the ischemic myocardium. The ASC secretome may have the ability to modulate the release of inflammatory cytokines, such as INF-γ, IDO, NO, IL-6, IL-8, IL-10, IL-11, and TNF-α. ASC-secreted factors such as IGF-1, VEGF, exosomes, and miR-301a may improve the capacity of cardiomyocyte survival in hypoxic conditions. Meanwhile, ASCs may secrete molecules such as VEGF, HGF, MCP-1, TIMP-1, and TIMP-4 that contribute to inhibiting fibrosis and cardiac remodeling. Maybe certain paracrine factors such as SDF-1, VEGF, FGF-2, HGF, CXCL-12, and microvesicles released by ASCs could recruit endogenous stem cells and enable cardiovacular lineage cells re-enter cell cycling. In addition, ASC-conditioned medium could induce conduction slowing of neonatal rat ventricular myocytes (NRVMs), probably attributed to the secondary autocrine myocardial factors released by NRVM