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REVIEW article
Front. Cell. Neurosci.
Sec. Cellular Neuropathology
Volume 18 - 2024 |
doi: 10.3389/fncel.2024.1470144
MAM-mediated mitophagy and endoplasmic reticulum stress: the hidden regulators of ischemic stroke
Provisionally accepted- 1 Heilongjiang University of Chinese Medicine, Harbin, Heilongjiang Province, China
- 2 First Affiliated Hospital of Heilongjiang University of Chinese Medicine, Harbin, China
Ischemic stroke (IS) is the predominant subtype of stroke and a leading contributor to global mortality. The mitochondrial-associated endoplasmic reticulum membrane (MAM) is a specialized region that facilitates communication between the endoplasmic reticulum and mitochondria, and has been extensively investigated in the context of neurodegenerative diseases. Nevertheless, its precise involvement in IS remains elusive. This literature review elucidates the intricate involvement of MAM in mitophagy and endoplasmic reticulum stress during IS. PINK1, FUNDC1, Beclin1, and Mfn2 are highly concentrated in the MAM and play a crucial role in regulating mitochondrial autophagy. GRP78, IRE1, PERK, and Sig-1R participate in the unfolded protein response (UPR) within the MAM, regulating endoplasmic reticulum stress during IS. Hence, the diverse molecules on MAM operate independently and interact with each other, collectively contributing to the pathogenesis of IS as the covert orchestrator.
Keywords: Mitochondrial-associated endoplasmic reticulum membrane(MAM), mitophagy, Endoplasmic Reticulum Stress, ischemic stroke(IS), unfolded protein response (UPR)
Received: 30 Jul 2024; Accepted: 12 Nov 2024.
Copyright: © 2024 Jia, Li, Xu, Li, Yang, Chen, Zhang, Li and Sun. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence:
Hongtao Li, First Affiliated Hospital of Heilongjiang University of Chinese Medicine, Harbin, China
Ruobing Li, Heilongjiang University of Chinese Medicine, Harbin, 150040, Heilongjiang Province, China
Long Chen, First Affiliated Hospital of Heilongjiang University of Chinese Medicine, Harbin, China
Qianwen Zhang, First Affiliated Hospital of Heilongjiang University of Chinese Medicine, Harbin, China
Shulin Li, First Affiliated Hospital of Heilongjiang University of Chinese Medicine, Harbin, China
XiaoWei Sun, First Affiliated Hospital of Heilongjiang University of Chinese Medicine, Harbin, China
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