miR-92a在脑缺血再灌注损伤中的机制研究与治疗进展OA
The mechanism of miR-92a in cerebral ischemia-reperfusion injury and therapy progress
脑缺血再灌注损伤(Cerebral ischemia-reperfusion injury,CIRI)是缺血性脑卒中及其他急性缺血相关疾病的重要病理环节,其机制涉及炎症反应、血脑屏障损伤、氧化应激及神经元凋亡等多种途径.miR-92a作为miR-17-92基因簇的关键成员,在神经血管单元(Neurovascular unit,NVU)的多种细胞类型(神经元、内皮细胞、周细胞及星形胶质细胞)中发挥重要调控作用.研究表明,miR-92a通过抑制Krüppel样因子2/4(Krüppel-like factor 2/4,KLF2/4)、神经调节蛋白1(Neuregulin 1,NRG1)及抗氧化相关分子(如HO-1、SIRT6)等表达,可加重炎症反应、血脑屏障功能障碍、氧化应激及神经元凋亡,从而加剧脑组织损伤.因此,针对miR-92a的功能和调节机制开发新的治疗策略,已成为CIRI研究领域的新方向.本文就miR-92a在CIRI中的多重调控机制进行综述,以期为脑卒中提供新的潜在治疗靶点与治疗思路.
Cerebral ischemia-reperfusion injury(CIRI)is a critical pathological process underlying ischemic stroke and other acute ischemic disorders.Its mechanisms involve inflammation,blood-brain barrier(BBB)disruption,oxidative stress,and neuronal apoptosis.As a key member of the miR-17-92 cluster,miR-92a plays an important regulatory role in multiple cell types of the neurovascular unit(NVU),including neurons,endothelial cells,pericytes,and astrocytes.Studies have shown that miR-92a aggravates inflammation,BBB dysfunction,oxidative stress,and neuronal apoptosis by inhibiting the expression of KLF2/4,NRG1,and antioxidative molecules such as HO-1 and SIRT6,thereby exacerbating brain injury.Therefore,developing new therapeutic strategies targeting the function and regulatory mechanisms of miR-92a has become a new focus in the field of CIRI research.This article reviews the multiple regulatory mechanisms of miR-92a in CIRI,aiming to provide new potential therapeutic targets and approaches for stroke.
钟惠敏;丁佳敏;陶爰名;黄宽;陈丽
赣南医科大学第一临床医学院赣南医科大学第一临床医学院赣南医科大学第一临床医学院赣南医科大学第一附属医院麻醉科,江西 赣州 341000赣南医科大学第一附属医院麻醉科,江西 赣州 341000
医药卫生
脑缺血再灌注损伤miR-92a脑卒中
Cerebral ischemia-reperfusion injurymiR-92aStroke
《赣南医科大学学报》 2026 (3)
195-199,5
江西省自然科学基金重点项目(20232ACB206050)
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