Department of Neurosurgery, The First Affiliated Hospital, Gannan Medical University, Ganzhou, Jiangxi, China.
Department of Endocrinology, The First Affiliated Hospital of Gannan Medical University, Ganzhou, Jiangxi, China.
Curr Neuropharmacol. 2024;23(1):85-97. doi: 10.2174/1570159X22666240704123701.
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.
缺血性脑卒中是全球范围内发病率和死亡率的重要原因。自噬是一种细胞内降解的过程,已被证明在缺血性脑卒中的发病机制中起着关键作用。长链非编码 RNA(lncRNA)已成为各种疾病中自噬的重要调节因子,包括缺血性脑卒中。最近的研究已经确定了几种 lncRNA 可以调节缺血性脑卒中中的自噬,包括 MALAT1、MIAT、SNHG12、H19、AC136007.2、C2dat2、MEG3、KCNQ1OT1、SNHG3 和 RMRP。这些 lncRNA 通过与自噬过程中涉及的关键蛋白相互作用来调节自噬,如 Beclin-1、ATG7 和 LC3。了解 lncRNA 在调节缺血性脑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点。