Tissue damage caused by ischemia-reperfusion (I/R) injury represents a serious event, which often leads to deterioration or even loss of organ function. I/R injury is associated with transient tissue oxygen deprivation due to vessel occlusion and a subsequent reperfusion period following restoration of blood flow. Initial tissue damage inflicted by ischemia is aggravated in the reperfusion period through mechanisms such as burst of reactive oxygen and nitrogen species and inflammatory reactions. I/R injury occurs during surgical interventions, organ transplantation, diseases such as myocardial infarction, circulatory shock, and toxic insults. Recently, microRNAs have come into focus as powerful regulators of gene expression and potential diagnostic tools during I/R injury. These small noncoding ribonucleotides (~22 nucleotides in length) posttranscriptionally target mRNAs, culminating in suppression of protein synthesis or increase in mRNA degradation, thus fundamentally influencing organ function. This review highlights the latest developments regarding the role of microRNAs in cardiac and renal I/R injury.
Keywords: CaMKII; DRP1; EPC; FGFR2; Free radicals; HIF-1α; Heart; Hsp20; I/R; Ischemia–reperfusion injury; KIF3B; Kidney; LIF; MV; MicroRNAs; Ncx1; PDCD4; PIO; PTEN; RISC; RNA-induced silencing complex; ROCK1; ROS; Rho-associated protein kinase 1; Sirt1; calmodulin kinase II; dynamin-related protein-1; endothelial progenitor cell; fibroblast growth factor receptor 2; heat shock protein 20; hypoxia-inducible factor 1α; ischemia–reperfusion; kinesin family member 3B; leukemia inhibitory factor; microvesicle; phosphatase and tensin homologue; pioglitazone; programmed cell death protein 4; reactive oxygen species; sirtuin 1; sodium/calcium exchanger 1.
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