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New insights into the role of mitochondrial dynamics in oxidative stress-induced diseases

The accumulation of excess reactive oxygen species (ROS) can lead to oxidative stress (OS), which can induce gene mutations, protein denaturation, and lipid peroxidation directly or indirectly. The expression is reduced ATP level in cells, increased cytoplasmic Ca2+, inflammation, and so on. Consequ...

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Bibliographic Details
Published in:Biomedicine & pharmacotherapy 2024-09, Vol.178, p.117084, Article 117084
Main Authors: Chen, Sisi, Li, Qilong, Shi, Hanjing, Li, Fengna, Duan, Yehui, Guo, Qiuping
Format: Article
Language:English
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Summary:The accumulation of excess reactive oxygen species (ROS) can lead to oxidative stress (OS), which can induce gene mutations, protein denaturation, and lipid peroxidation directly or indirectly. The expression is reduced ATP level in cells, increased cytoplasmic Ca2+, inflammation, and so on. Consequently, ROS are recognized as significant risk factors for human aging and various diseases, including diabetes, cardiovascular diseases, and neurodegenerative diseases. Mitochondria are involved in the production of ROS through the respiratory chain. Abnormal mitochondrial characteristics, including mitochondrial OS, mitochondrial fission, mitochondrial fusion, and mitophagy, play an important role in various tissues. However, previous excellent reviews focused on OS-induced diseases. In this review, we focus on the latest progress of OS-induced mitochondrial dynamics, discuss OS-induced mitochondrial damage-related diseases, and summarize the OS-induced mitochondrial dynamics-related signaling pathways. Additionally, it elaborates on potential therapeutic methods aimed at preventing oxidative stress from further exacerbating mitochondrial disorders. [Display omitted] •Oxidative stress induces mitochondrial dynamics.•Oxidative stress leads to mitochondrial damage-related diseases.•Assembles mitochondrial reactive oxygen species related signaling pathways.•Natural plant extracts is effective for mitochondrial damage-related disease treatment.
ISSN:0753-3322
1950-6007
1950-6007
DOI:10.1016/j.biopha.2024.117084