Cav3.2 deletion attenuates nonalcoholic fatty liver disease in mice

•Cav3.2 knockout (Cav3.2 KO) improves hepatic steatosis, liver injury and metabolic syndrome in NAFLD mice model.•Further studies showed that Cav3.2 KO inhibited HFD-induced hepatic oxidative stress, inflammation and hepatocyte apoptosis.•We found that Cav3.2 KO also attenuated the hepatic lipid acc...

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Veröffentlicht in:	Gene 2024-12, Vol.929, p.148812, Article 148812
Hauptverfasser:	Li, Xue, Hu, Chengyun, Luo, Shanshan, Dai, Feibiao, Li, Chuanyao, Zhou, Wanjun, Wang, Jiawu, Chen, Hao, Wang, Zhen, Long, Tengfei, Jiang, Lai, Tang, Chaoliang
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Apoptosis calcium channels Calcium Channels, T-Type - genetics Calcium Channels, T-Type - metabolism Cav3.2 Diet, High-Fat - adverse effects Disease Models, Animal energy fatty liver genes hepatocytes Hepatocytes - metabolism Hepatocytes - pathology hepatoma Inflammation Inflammation - genetics Inflammation - metabolism liver Liver - metabolism Liver - pathology liver cirrhosis Male metabolic syndrome Mice Mice, Inbred C57BL Mice, Knockout Non-alcoholic Fatty Liver Disease - genetics Non-alcoholic Fatty Liver Disease - metabolism Non-alcoholic Fatty Liver Disease - pathology Nonalcoholic fatty liver disease oleic acid Oxidative Stress palmitic acid therapeutics
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