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MAM-mediated mitophagy and endoplasmic reticulum stress: the hidden regulators of ischemic stroke
Ziyi Jia1, Hongtao Li2, Ke Xu3
1The First Clinical Medical College, Heilongjiang University of Chinese Medicine, Harbin, China.
Abstract:
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.
Insights
The mitochondrial-associated endoplasmic reticulum membrane (MAM) plays a key role in ischemic stroke (IS) by regulating mitophagy and endoplasmic reticulum stress. Understanding MAM
Area of Science:
- Neuroscience
- Cell Biology
- Pathology
Background:
- Ischemic stroke (IS) is a major cause of death globally.
- The mitochondrial-associated endoplasmic reticulum membrane (MAM) is crucial for cell communication but its role in IS is unclear.
Purpose of the Study:
- To review the role of MAM in mitophagy and endoplasmic reticulum stress in ischemic stroke.
- To identify key molecules involved in MAM-mediated pathogenesis of IS.
Main Methods:
- Literature review of studies on MAM, mitophagy, endoplasmic reticulum stress, and ischemic stroke.
- Analysis of the roles of specific proteins (PINK1, FUNDC1, Beclin1, Mfn2, GRP78, IRE1, PERK, Sig-1R) in MAM during IS.
Main Results:
- MAM regulates mitophagy via proteins like PINK1, FUNDC1, Beclin1, and Mfn2.
- MAM mediates endoplasmic reticulum stress through UPR proteins such as GRP78, IRE1, PERK, and Sig-1R.
- These molecules interact within the MAM to influence IS pathogenesis.
Conclusions:
- The MAM is a critical regulator of cellular processes involved in ischemic stroke.
- MAM-associated proteins orchestrate mitophagy and endoplasmic reticulum stress, contributing to IS development.
- Targeting MAM pathways may offer novel therapeutic strategies for ischemic stroke.
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