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. Author manuscript; available in PMC: 2014 Jan 9.
Published in final edited form as: Nat Med. 2011 Nov 7;17(11):10.1038/nm.2507. doi: 10.1038/nm.2507

Figure 5.

Figure 5

MiRNA pathways implicated in myocardial ischemia and reperfusion. miR-92a (encoded by the miR-17-92a cluster) is highly expressed in vascular endothelia, and blocks ischemic angiogenesis by inhibition of proangiogenic proteins such as the α5 integrin (encoded by ITGA5). In contrast, miR-499 and miR-24 levels are repressed in cardiac tissue following ischemia and reperfusion. MiR-499 suppresses myocyte apoptosis by direct repression of calcineurin subunit synthesis, leading to decreased calcineurin-mediated dephosphorylation of DRP1, thereby interfering with DRP1-mediated activation of the pro-apoptotic mitochondrial fission program. MiR-24 inhibits myocyte apoptosis by direct repression of BIM synthesis. Accordingly, decreasing miR-92a levels (therapeutic inhibition) or increasing miR-499 or miR-24 levels (therapeutic enhancement) might have beneficial effects in the setting of myocardial ischemia and reperfusion. CN, calcineurin; EC, endothelial cell.