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Alcoholic liver disease is the major cause of chronic liver diseases. Excessive alcohol intake results in endoplasmic reticulum (ER) stress. ERdj5, a member of DNAJ family, is an ER-resident chaperone protein, whose role in alcoholic liver disease remains to be investigated. In this study, we aim to address the effect of ERdj5 on alcoholic liver disease and the underlying mechanism. Hepatic Dnajc10 (ERdj5) mRNA expression was elevated in both human and mouse alcoholic hepatitis. In mice subjected to chronic and binge ethanol feeding, ERdj5 levels were also markedly increased. Hepatic Dnajc10 correlated with Xbp1s mRNA. Tunicamycin, an ER stress inducer, increased ERdj5 levels. Dnajc10 knockout mice exhibited exacerbated alcohol-induced liver injury and hepatic steatosis. However, the macrophage numbers and chemokine levels were similar to those in wild-type mice. Depletion of Dnajc10 promoted oxidative stress. Ethanol feeding increased hepatic H

Liver cirrhosis is characterized by the extensive deposition of extracellular matrix such as fibril collagen, causing dysfunction and failure of the liver. Hepatic macrophages play pivotal roles in the transition from inflammatory to restorative properties upon hepatic injury. In particular, scar-associated macrophages (SAMacs) control liver fibrosis with the representative expression of matrix metalloproteinase (MMP). However, the heterogenic SAMac population has not been well characterized yet. Here, we profiled heterogeneous liver macrophages using public databases of single-cell transcriptomics and found TIM4