Обзорная статья

Ischemic Stroke and Autophagy: The Roles of Long Non-Coding RNAs

Long-qiang OuyangDepartment of Neurosurgery, The First Affiliated Hospital, Gannan Medical University, Ganzhou, Jiangxi, ChinaWenyan XiaDepartment of Endocrinology, The First Affiliated Hospital of Gannan Medical University, Ganzhou, Jiangxi, ChinaAmeen Abdulhasan Al-AlwanyDepartment of Medicine, College of Medicine, Baghdad University, Baghdad, IraqReena GuptaInstitute of Pharmaceutical Research, GLA University, Mathura, Uttar Pradesh, 281406, IndiaI.B. SapaevNew Uzbekistan University, Tashkent, UzbekistanSami G. AlmalkiDepartment of Medical Laboratory Sciences, College of Applied Medical Sciences, Majmaah University, Majmaah 11952, Saudi ArabiaSaud AlmawashDepartment of Pharmaceutical Sciences, College of Pharmacy, Shaqra University, Shaqra, Saudi ArabiaRand Ali ZiyadCollege of Pharmacy, National University of Science and Technology, Dhi Qar, IraqAhmed AlawadiCollege of Technical Engineering, The Islamic University of Babylon, IraqAli AlsalamyCollege of Technical Engineering, Imam Ja’afar Al‐Sadiq University, Al‐Muthanna 66002, Iraq

Current Neuropharmacologyjournal2024en

ABI

Аннотация

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.

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Темы

Идентификаторы

DOI: 10.2174/1570159x22666240704123701

Цитирования и источники

Цитирований: 1 Использованных источников: 115

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