Abstract
Ischemic stroke is a cerebrovascular disease with high mortality and disability, which seriously affects the health and lives of people around the world. Effective treatment for ischemic stroke has been limited by its complex pathological mechanisms. Increasing evidence has indicated that mitochondrial dysfunction plays an essential role in the occurrence, development, and pathological processes of ischemic stroke. Therefore, strict control of the quality and quantity of mitochondria via mitochondrial fission and fusion as well as mitophagy is beneficial to the survival and normal function maintenance of neurons. Under certain circumstances, excessive mitophagy also could induce cell death. This review discusses the dynamic changes and double-edged roles of mitochondria and related signaling pathways of mitophagy in the pathophysiology of ischemic stroke. Furthermore, we focus on the possibility of modulating mitophagy as a potential therapy for the prevention and prognosis of ischemic stroke. Notably, we reviewed recent advances in the studies of natural compounds, which could modulate mitophagy and exhibit neuroprotective effects, and discussed their potential application in the treatment of ischemic stroke.
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References
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This work was supported by the National Natural Science Foundation of China (NO.82174047, 81622051), Zhejiang Provincial Natural Science Foundation of China (NO.LY22H280004) and Foundation of Zhejiang Chinese Medical University (No.2020ZR20).
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All authors contributed to the study conception and design. MS and XF conceived and designed the review. MS did the literature searches, did data interpretation, and manuscript writing. YZ did manuscript writing and developed the figure. XF reviewed and revised the manuscript. All authors read and approved the final manuscript.
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Song, M., Zhou, Y. & Fan, X. Mitochondrial Quality and Quantity Control: Mitophagy Is a Potential Therapeutic Target for Ischemic Stroke. Mol Neurobiol 59, 3110–3123 (2022). https://doi.org/10.1007/s12035-022-02795-6
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DOI: https://doi.org/10.1007/s12035-022-02795-6