Table 3.

Summary of selected microRNAs with known altered expression profiles in IRI-associated AKI, which contributes to the pathogenesis of renal injury.

MicroRNA	Impact of Ischemia-Reperfusion Injury on Expression in Renal Tissue/Cells	Mechanism Linking to Acute Kidney Injury	References
miR-182	Increased	miR-182 enhances apoptosis of tubular epithelial cells through targeting FoxO3.	[101]
miR-132-3p	Increased	miR-132-3p targets SIRT1 and further deteriorates oxidative balance in ischemia.	[104]
miR-21	Increased	miR-21 plays a protective role in IRI-associated AKI by suppressing dendritic cell maturation, thus limiting the inflammatory responses.	[105]
miR-211	Decreased	Through inhibiting TGF-β/SMAD signaling, miR-211 improves cell viability.	[109]
miR-192-5p	Increased	Suppression of miR-192-5p improved viability of renal cells under hypoxia/reoxygenation conditions. The molecule targets FTO.	[110]
miR-187	Decreased	Increasing the expression of miR-187 reduces podocyte damage.	[111]
miR-194	Decreased	By targeting Rheb, miR-194 reduces inflammation and oxidative stress in renal cells stimulated by hypoxia and reoxygenation.	[112]