长链非编码RNA在脑缺血再灌注损伤中调控神经元细胞自噬的研究进展

Research progress of long non-coding RNA involved in autophagy regulation in cerebral ischemia-reperfusion injury

目前长链非编码RNA(long noncoding RNA,lncRNA)已成为治疗脑缺血再灌注损伤的新靶标。越来越多的证据表明,lncRNA可以通过影响神经元细胞自噬参与脑缺血再灌注损伤的调节。文章从自噬的角度,以“lncRNA”、“神经元自噬”和“脑缺血再灌注损伤”等作为关键词,系统回顾了lncRNA介导的神经元细胞自噬在脑缺血再灌注损伤中的相关研究。结果表明,lncRNA可以在自噬的各个阶段(诱导、成核、延伸、成熟和自噬体裂解)调控重要分子靶点,从而调节细胞自噬水平发挥神经保护作用。深入了解lncRNA在脑缺血再灌注损伤中自噬的调节机制,有望为缺血性脑损伤的治疗带来新的希望。

At present,long noncoding RNA(lncRNA)have become a new target for the treatment of cerebral ischemia-reperfusion injury. Accumulating evidence demonstrates that the lncRNA can participate in the regulation of cerebral ischemia-reperfusion injury by affecting neuronal cell autophagy. This article aims to systematically review the effects of lncRNA-mediated neuronal cell autophagy in brain deficiency from the perspective of autophagy,using“lncRNA”,“neuronal autophagy”and“cerebral ischemia-reperfusion injury”as keywords. Studies have shown that lncRNA can regulate important target genes at all stages of autophagy(induction,nucleation,extension,maturation,and autophagosome lysis),thereby regulating the level of autophagy and exerting neuroprotective effects. Understanding the autophagy regulation of lncRNA and its mechanism of action in cerebral ischemia-reperfusion injury is expected to bring new hope for the treatment of ischemic brain injury.