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. Author manuscript; available in PMC: 2022 Nov 1.
Published in final edited form as: Pharmacol Res. 2021 Sep 23;173:105912. doi: 10.1016/j.phrs.2021.105912

Fig. 3. IL-10 helps in cardiac regeneration and protects the heart via alleviating inflammation and apoptosis.

Fig. 3.

IL-10 inhibits miR-375 which upregulates PDK1/AKT pathway and increases angiogenesis and cell survival of bone marrow angiogenic progenitor cells (BMAPC). The miR-375 inhibition in BMAPC increases its survival after transplantation in the heart following MI. This suggests how IL-10 can protect the heart following MI via downregulating miR-375. Following MI, the level of SDF-1 decreases which reduces bone marrow progenitor cell mobilization and homing to the heart that impairs cardiac regeneration. Exogenous administration of IL-10 increases the expression of SDF-1 which helps in the movement of bone marrow progenitor cells and improves cardiac function in an infarcted heart. The deletion of HuR protein in macrophage reduces the level of TNFα, p53 and TGF-β following inflammatory insult. Upon binding of HuR to AU-rich elements (AREs) in the 3 untranslated regions of mRNA of inflammatory cytokine, including IL-1β and TNFα, stabilizes the cytokines which augments cardiac inflammation. HuR also promotes apoptosis via p53 signaling and augments fibrosis via activation of TGF-β. IL-10 inhibits HuR and, therefore, reduces cardiac inflammation, apoptosis and fibrosis. In IL-10 KO mice, the deletion of HuR alleviates cardiac dysfunction. IL-10 also inhibits the movement of bone marrow fibroblast progenitor cells following pressure overload-induced hypertrophy and minimizes cardiac fibrosis.