Mitophagy in relation to chronic inflammation/ROS in aging
- PMID: 38834837
- DOI: 10.1007/s11010-024-05042-9
Mitophagy in relation to chronic inflammation/ROS in aging
Abstract
Various assaults on mitochondria occur during the human aging process, contributing to mitochondrial dysfunction. This mitochondrial dysfunction is intricately connected with aging and diseases associated with it. In vivo, the accumulation of defective mitochondria can precipitate inflammatory and oxidative stress, thereby accelerating aging. Mitophagy, an essential selective autophagy process, plays a crucial role in managing mitochondrial quality control and homeostasis. It is a highly specialized mechanism that systematically removes damaged or impaired mitochondria from cells, ensuring their optimal functioning and survival. By engaging in mitophagy, cells are able to maintain a balanced and stable environment, free from the potentially harmful effects of dysfunctional mitochondria. An ever-growing body of research highlights the significance of mitophagy in both aging and age-related diseases. Nonetheless, the association between mitophagy and inflammation or oxidative stress induced by mitochondrial dysfunction remains ambiguous. We review the fundamental mechanisms of mitophagy in this paper, delve into its relationship with age-related stress, and propose suggestions for future research directions.
Keywords: Aging; Chronic inflammation; Mitophagy; ROS.
© 2024. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.
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References
-
- Guo J, Huang X, Dou L, Yan M, Shen T, Tang W, Li J (2022) Aging and aging-related diseases: from molecular mechanisms to interventions and treatments. Signal Transduct Target Ther 7(1):391. https://doi.org/10.1038/s41392-022-01251-0 - DOI - PubMed - PMC
-
- Wu Z, Qu J, Zhang W, Liu GH (2023) Stress, epigenetics, and aging: unraveling the intricate crosstalk. Mol Cell. https://doi.org/10.1016/j.molcel.2023.10.006 - DOI - PubMed - PMC
-
- Yu CH, Davidson S, Harapas CR, Hilton JB, Mlodzianoski MJ, Laohamonthonkul P, Louis C, Low RRJ, Moecking J, De Nardo D, Balka KR, Calleja DJ, Moghaddas F, Ni E, Mclean CA, Samson AL, Tyebji S, Tonkin CJ, Bye CR, Turner BJ, Pepin G, Gantier MP, Rogers KL, Mcarthur K, Crouch PJ, Masters SL (2020) TDP-43 triggers mitochondrial DNA release via mPTP to activate cGAS/STING in ALS. Cell 183(3):636-649.e618. https://doi.org/10.1016/j.cell.2020.09.020 - DOI - PubMed - PMC
-
- Wang Y, Li N, Zhang X, Horng T (2021) Mitochondrial metabolism regulates macrophage biology. J Biol Chem 297(1):100904. https://doi.org/10.1016/j.jbc.2021.100904 - DOI - PubMed - PMC
-
- Miwa S, Kashyap S, Chini E, Von Zglinicki T (2022) Mitochondrial dysfunction in cell senescence and aging. J Clin Invest. https://doi.org/10.1172/jci158447 - DOI - PubMed - PMC
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