Abstract
Ischemia-reperfusion (I/R) injury is a progressive injury that aggravates the pathological state when the organ tissue restores blood supply after a certain period of ischemia, including the myocardial, brain, liver, kidney, and intestinal. With growing evidence that microRNAs (miRNAs) play an important role as posttranscription gene silencing mediators in many I/R injury, in this review, we highlight the microRNAs that are related to I/R injury and their regulatory molecular pathways. In addition, we discussed the potential role of miRNA as a biomarker and its role as a target in I/R injury treatment. Developing miRNAs are not without its challenges, but prudent design combined with existing clinical treatments will result in more effective therapies for I/R injury. This review is aimed at providing new research results obtained in this research field. It is hoped that new research on this topic will not only generate new insights into the pathophysiology of miRNA in I/R injury but also can provide a basis for the clinical application of miRNA in I/R.
Highlights
Mature microRNA is a small but noncoding single-stranded RNA molecule with mature transcripts of 18-25 nucleotides
The initial transcript of miRNA is a long RNA transcript containing at least one hairpin-shaped miRNA precursor, which has a short existence time. It is cut by Ribonuclease III (RNase III) endonuclease and/or splicing elements similar to Drosha to form a 60-70 nt premiRNA with stem ring structure [5]. This structure is transported from the nucleolus into the cytoplasm by Exportin-5, a guanosine triphosphate- (GTP-) bound form(RanGTP-) dependent double-stranded RNA binding protein that mediates the nuclear output of miRNAs
The therapies based on miRNA have achieved remarkable results in various I/R injury in vivo and in vitro
Summary
Mature microRNA (miRNA) is a small but noncoding single-stranded RNA molecule with mature transcripts of 18-25 nucleotides. A recent study showed that mice treated with necrosis-related factor (Nrf) siRNA showed a decrease in the AMI area and an improvement in cardiac function during MI/RI [81] These studies show that downregulation of miRNAs through siRNAs may be a promising tool for the treatment of ischemic diseases. Wang et al [92] administered lentivirus carrying miR-214 to reduce the area of AMI after I/R injury by targeting the expression of Bri1-Ems-Suppressor1(BES1-) interacting Myc-like protein-1 (Bim1) and preventing its transfer from cytoplasm to mitochondria in vivo and vitro This significantly reduced the apoptosis of myocardial cells induced by I/R and further protected the heart from I/R injury without toxicity. Because miRNA mimetics have no carrier toxicity, if the drug delivery system was verified to have no side effects after long-term use, it will be a promising therapy for anti-ischemic diseases
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