粒体自噬
衰老
氧化应激
氮氧化物4
细胞生物学
自噬
磷脂病
线粒体
线粒体ROS
活性氧
化学
生物
生物化学
NADPH氧化酶
细胞凋亡
磷脂
膜
作者
Jie‐Ru Hong,Chen‐Yu Zhang,Wenjing Zhong,Hui‐Hui Yang,Jian‐Bing Xiong,Ping Deng,Nan-Shi-Yu Yang,Hui Cai,Ling Jin,Cha‐Xiang Guan,Jia‐Xi Duan,Yong Zhou
标识
DOI:10.1016/j.biopha.2023.115937
摘要
Alveolar epithelial cell (AEC) senescence is considered to be a universal pathological feature of many chronic pulmonary diseases. Our previous study found that epoxyeicosatrienoic acids (EETs), produced from arachidonic acid (ARA) through the cytochrome P450 cyclooxygenase (CYP) pathway, have significant negative regulatory effects on cellular senescence in AECs. However, the exact mechanisms by which EETs alleviate the senescence of AECs still need to be further explored. In the present study, we observed that bleomycin (BLM) induced enhanced mitophagy accompanied by increased mitochondrial ROS (mito-ROS) content in the murine alveolar epithelial cell line MLE12. While EETs reduced BLM-induced mitophagy and mito-ROS content in MLE12 cells, and the mechanism was related to the regulation of NOX4/Nrf2-mediated redox imbalance. Furthermore, we found that inhibition of EETs degradation could significantly inhibit mitophagy and regulate NOX4/Nrf2 balance to exert anti-oxidant effects in D-galactose-induced premature aging mice. Collectively, these findings may provide new ideas for treating age-related pulmonary diseases by targeting EETs to improve mitochondrial dysfunction and reduce oxidative stress.
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