Table 1.

miRNAs associated with cardiac ischemia which might be manipulated for attenuating several aspects of myocardial injury (apoptosis, necrosis, fibrosis, and neovascularization) or improving regenerative therapies

miRNA	Attenuation of myocardial injury				Regenerative applications
	Cardiomyocyte apoptosis	Necrosis	Fibrosis	Neovascularization
miR-1	Repression of antiapoptotic Bcl2 [76], Igf1 [47, 75], Hsp60, Hsp70 [77]		Targeting of profibrotic Fibullin-2 [87]	Enhanced tubulogenesis by repressing Spred-1 [96]
miR-15	Repression of antiapoptotic Bcl2 [74]				Inhibition of cardiomyocyte proliferation [144, 145]
miR-21	Protection against apoptosis by targeting Pdcd4 [55, 57, 58]	Reduced necrosis in cultured cardiomyocytes [57]	Promotion of fibroblast proliferation and inhibition of metalloprotease [80, 81, 83], promotion of TGFβ [91]		Improved engraftment of transplanted cardiac progenitor cells [59]
miR-24	Suppression of apoptosis, by repression of Bim [54]	Reduced necrosis in cultured ischemic cardiomyocytes [56]	Decreased fibroblast differentiation and migration by targeting Tgfβ [92]	Inhibition of proangiogenic Gata2 and Pak4 [101]	Improved engraftment of transplanted cardiac progenitor cells [59]
miR-29	Proapoptotic by targeting Mcl-1 [73]		Targeting of fibrotic proteins[86]
miR-30	Inhibition of mitochondrial fission by suppressing Drp1 [53]		Decreased production of collagens[85]
miR-34	Proapoptotic targeting of Pnuts [72]
miR-92				Inhibition of the proangiogenic Itga5 [100]	Induction of cardiomyocyte proliferation [151]
miR-101			Decreased fibroblast proliferation and collagen deposition by targeting Tgf-β signaling [93]
miR-126				Increased proliferation and migration of endothelial cells by repressing Spred-1 [95]	Increased angiogenesis after mesenchymal stem cells [97, 98] and endothelial progenitors [99] trasplantation
miR-133	Repressing proapoptotic Caspase 9 [77]		Decreased production of collagens [85]		Increased regeneration in zebrafish [147]
miR-145	Attenuation of Calcium overload by repressing CaMKIIδ [113] and Bnip3 [114]
miR-199 and 590					Induction of cell cycle reentry [152]
miR-210	Inhibition of apoptosis by targeting Ptp1b [64]			Enhanced angiogenesis by repression of Efna3 [62]	Increased engraftment of bone marrow-derived stem cells [65] and increased survival of mesenchymal stem cells [18]
miR-214	Attenuation of calcium overload by repressing Ncx1 and CaMKIIδ [112]	Attenuation of calcium overload [112]		Inhibition of endothelial cells sprouting [102]
miR-221					Improved engraftment of transplanted cardiac progenitor cells [59]
miR-320	Proapoptotic by targeting Hsp20 [69]
miR-378	Targeting antiapoptotic Igf1R [48] but also apoptotic Caspase 3 [78]	Inhibition of necrosis in hypoxic cardiomyocytes [78]
miR-494	Activation of Akt [79]	Reduced necrotic death after I/R [79]
miR-499	Inhibition of mitochondrial fission [52]				Increased regenerative potential and differentiation of cardiac progenitors[17]
miR-711			Targeting Sp1, reducing collagen production[88]

Detrimental effects are shown in italics