ER stress promotes mitochondrial calcium overload and activates the ROS/NLRP3 axis to mediate fatty liver ischemic injury.

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作者： Fei,Li ^[1] ; Zhu,Guan ^[1] ; Yiyun,Gao ^[2] ; Yan,Bai ^[1] ; Xinyu,Zhan ^[2] ; Xingyue,Ji ^[1] ; Jian,Xu ^[2] ; Haoming,Zhou ^[2] ; Zhuqing,Rao ^[1]

作者单位： Department of Anesthesiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China. ^[1] Hepatobiliary Center, The First Affiliated Hospital of Nanjing Medical University; Key Laboratory of Liver Transplantation, Chinese Academy of Medical Sciences; NHC Key Laboratory of Living Donor Liver Transplantation, Nanjing Medical University, Nanjing, China. ^[2]

主题词动物(Animals);人类(Humans);小鼠(Mice);钙(Calcium);脂肪肝(Fatty Liver);炎症(Inflammation);缺血(Ischemia);活性氧(Reactive Oxygen Species)

DOI 10.1097/HC9.0000000000000399

PMID 38497930

发布时间 2024-10-03

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Hepatology communications

2024年8卷4期

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ER stress promotes mitochondrial calcium overload and activates the ROS/NLRP3 axis to mediate fatty liver ischemic injury.

Hepatology communications

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Hepatology communications

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ER stress promotes mitochondrial calcium overload and activates the ROS/NLRP3 axis to mediate fatty liver ischemic injury.

Hepatology communications

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Hepatology communications

相关期刊

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