MiRNA Regulating Autophagy Signaling Pathway Induced by Cerebral Ischemia/Reperfusion
10.13471/j.cnki.j.sun.yat-sen.univ(med.sci).20240004.003
- VernacularTitle:MiRNA调控脑缺血/再灌注诱导的自噬信号通路研究进展
- Author:
Xiaoai LIU
1
;
Yougen LUO
2
Author Information
1. Institute of Nursing， Guangdong Food and Drug Vocational College， Guangzhou 510520， China
2. Yancheng Hemiplegia Rehabilitation Engineering Technology Research Center， Jiangsu Vocational College of Medicine， Yancheng 224005， China
- Publication Type:Review
- Keywords:
cerebral ischemia reperfusion injury;
MicroRNA;
autophagy;
signal pathway;
autophagy related proteins;
regulation
- From:
Journal of Sun Yat-sen University(Medical Sciences)
2024;45(1):21-27
- CountryChina
- Language:Chinese
-
Abstract:
Ischemia and hypoxia cause functional damage to brain tissues during stroke， and when blood supply is restored to brain tissues after ischemia， a large number of free radicals and calcium overload cause cerebral ischemia-reperfusion injury， which further aggravates the condition. Autophagy is a self-protection mechanism that maintains the homeostasis of the intracellular environment， but excessive autophagy causes brain tissue damage. MiRNA is a small endogenous non-coding RNA molecule that regulate various physiological activities at the gene level by binding to complementary sequences in the 3 '- UTR of its target gene mRNA， leading to translation inhibition or mRNA degradation. MiRNA not only directly acts on autophagy related proteins， but also participates in autophagy regulation induced by ischemia/reperfusion through various signaling pathways. However， there is still a lack of systematic induction and analysis of miRNA regulation of autophagy signaling pathways induced by cerebral ischemia/reperfusion. This article reviews the regulation of cellular autophagy during cerebral ischemia/ reperfusion by miRNA-124， miRNA-298， miRNA-202-5p， miRNA-142， miRNA-26b and so on through different signaling pathways， providing a systematic and theoretical approach for the study of autophagy in stroke.
