Parkin-mediated mitochondrial quality control protects against aluminum-induced liver damage in mice
Parkin-mediated mitochondrial quality control protects against aluminum-induced liver damage in mice
复制标题
Parkin介导的线粒体质量控制可防止铝诱导的小鼠肝损伤
DOI：
10.1016/j.fct.2021.112485
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发表时间：
2021
影响因子：
4.3
通讯作者：
Yanfei Li
中科院分区：
文献类型：
--
作者：
Bonan Xiao;Yilong Cui;Yuping Wang;Menglin Liu;Pengli Liu;Jian Zhang;Xuliang Zhang;Miao Song;Yanfei Han;Yanfei Li
Aluminum (Al) is known to be hepatotoxic. Oxidative stress is the main mechanism of liver injury caused by Al, and can also lead to mitochondrial damage. Mitochondrial damage is a prerequisite for mitochondrial quality control (MQC) dysregulation. Parkin can activate MQC and maintain mitochondrial homeostasis. However, the role of Parkin-mediated MQC in Al-induced liver damage has not been elucidated. In this study, forty male wild type (WT) C57BL/6N mice were treated with 0, 44.825, 89.65 or 179.3 mg/kg body weight AlCl3in drinking water for 90 days, respectively. We found that Al induced mitophagy and disrupted mitochondrial dynamics and mitochondrial biogenesis. Then, twenty male WT C57BL/6N mice and twenty male Parkin knockout (Parkin−/-) C57BL/6N mice were divided into four groups and treated with 0, 89.65, 0, 89.65 mg/kg body weight AlCl3in drinking water for 90 days, respectively. We found that Parkin−/-inhibited mitophagy and further disrupted mitochondrial dynamics and mitochondrial biogenesis. These results indicated that Parkin-mediated MQC could be disrupted by Al and protected against Al-induced liver damage.
