MCU Upregulation Overactivates Mitophagy by Promoting VDAC1 Dimerization and Ubiquitination in the Hepatotoxicity of Cadmium

• Published in: Advanced science Vol. 10; no. 7; pp. e2203869 - n/a
• Main Authors: Liu, Cong, Li, Hui‐Juan, Duan, Wei‐Xia, Duan, Yu, Yu, Qin, Zhang, Tian, Sun, Ya‐Pei, Li, Yuan‐Yuan, Liu, Yong‐Sheng, Xu, Shang‐Cheng
• Format: Journal Article
• Language: English
• Published: Germany John Wiley & Sons, Inc 01.03.2023; John Wiley and Sons Inc; Wiley
• Subjects: Animals; Apoptosis; Autophagy; cadmium; Cadmium - toxicity; Calcium Channels - genetics; Calcium Channels - metabolism; Chemical and Drug Induced Liver Injury - metabolism; Dimerization; hepatotoxicity; Homeostasis; Kinases; Liver cancer; Mice; Microscopy; Mitochondria; mitochondrial calcium uniporter; Mitochondrial Proteins - genetics; Mitochondrial Proteins - metabolism; mitophagy; Mitophagy - genetics; Mitophagy - physiology; Protein expression; Proteins; Ubiquitination; Up-Regulation; Voltage-Dependent Anion Channel 1 - metabolism; voltage‐dependent anion‐selective channel protein 1; mitochondrial calcium uniporter; cadmium; mitophagy; voltage-dependent anion-selective channel protein 1; hepatotoxicity

Cadmium (Cd) is a high‐risk pathogenic toxin for hepatic diseases. Excessive mitophagy is a hallmark in Cd‐induced hepatotoxicity. However, the underlying mechanism remains obscure. Mitochondrial calcium uniporter (MCU) is a key regulator for mitochondrial and cellular homeostasis. Here, Cd exposure...