Abstract：
Ischemic stroke is a significant cause of morbidity and mortality worldwide. Autophagy, a process of intracellular degradation, has been shown to play a crucial role in the pathogenesis of ischemic stroke. Long non-coding RNAs (lncRNAs) have emerged as essential regulators of autophagy in various diseases, including ischemic stroke. Recent studies have identified several lncRNAs that modulate autophagy in ischemic stroke, including MALAT1, MIAT, SNHG12, H19, AC136007. 2, C2dat2, MEG3, KCNQ1OT1, SNHG3, and RMRP. These lncRNAs regulate autophagy by interacting with key proteins involved in the autophagic process, such as Beclin-1, ATG7, and LC3. Understanding the role of lncRNAs in regulating autophagy in ischemic stroke may provide new insights into the pathogenesis of this disease and identify potential therapeutic targets for its treatment.
摘要：
缺血性中风是世界范围内发病率和死亡率的重要原因。自噬,细胞内降解的过程，已被证明在缺血性卒中的发病机制中起着至关重要的作用。长链非编码RNA（lncRNAs）已成为各种疾病中自噬的重要调节因子，包括缺血性中风.最近的研究已经确定了几种调节缺血性卒中自噬的lncRNAs,包括MALAT1MIAT,SNHG12、H19、AC136007。2、C2dat2、MEG3、KCNQ1OT1、SNHG3和RMRP。这些lncRNAs通过与参与自噬过程的关键蛋白相互作用来调节自噬，例如Beclin-1、ATG7和LC3。了解lncRNAs在调节缺血性卒中自噬中的作用可能为该疾病的发病机制提供新的见解，并确定其治疗的潜在治疗靶标。
