Table 1.

A list of miRNAs implicated in diabetes that potentially modulate I/R injury via various mechanisms.

miRNA	Function	Level in Diabetes
miR-34	silences sirtuin-1 promotes apoptosis induces senescence exacerbates I/R injury	increased
miR-144	alleviates diabetic oxidative stress decreases in I/R injury mitigates oxygen-glucose I/R-induced injury promotes autophagy improves cardiomyocyte survival and promotes cardioprotection	decreased
miR-210	may elicit an anti-apoptotic effect worsens hypoxia-induced I/R injury increases or decreases apoptosis (depending on model; see text for details) promotes autophagy in endometrial cells	increased
miR-141	can promote or inhibit autophagy likely attenuates myocardial injury likely increases ROS in diabetic hearts	increased
miR-155	increases ROS worsens cardiac fibrosis in the diabetic MI mouse model promotes autophagy	increased
miR-21	protects against hypoxia-induced apoptosis promotes the post-conditioning protective effects in a myocardial I/R diabetic rat model decreases autophagy in myocardial tissue	increased
miR-146	inhibits hypoxia-induced apoptosis promotes the therapeutic potential of stem cells in the I/R-injured heart decreases inflammation and reduces oxidative stress induces senescence of endothelial cells inhibits autophagy	increased
miR-200b	prevents diabetes-induced adverse myocardial structural and functional changes	decreased
miR-200c	increases ROS decreases NO formation contributes to vascular dysfunction is upregulated in ischemia is linked to enhanced myocardial I/R injury in diabetes	increased