Corrigendum
Open Access | 
10.1172/jci.insight.197929
Chronic-plus-binge alcohol intake induces production of proinflammatory mtDNA-enriched extracellular vesicles and steatohepatitis via ASK1/p38MAPKα-dependent mechanisms
Jing Ma, Haixia Cao, Robim M. Rodrigues, Mingjiang Xu, Tianyi Ren, Yong He, Seonghwan Hwang, Dechun Feng, Ruixue Ren, Peixin Yang, Suthat Liangpunsakul, Jian Sun, and Bin Gao
Find articles by Ma, J. in: PubMed | Google Scholar
Find articles by Cao, H. in: PubMed | Google Scholar
Find articles by Rodrigues, R. in: PubMed | Google Scholar
Find articles by Xu, M. in: PubMed | Google Scholar
Find articles by Ren, T. in: PubMed | Google Scholar
Find articles by He, Y. in: PubMed | Google Scholar
Find articles by Hwang, S. in: PubMed | Google Scholar
Find articles by
Feng, D.
in:
PubMed
|
Google Scholar
|
Find articles by Ren, R. in: PubMed | Google Scholar
Find articles by Yang, P. in: PubMed | Google Scholar
Find articles by
Liangpunsakul, S.
in:
PubMed
|
Google Scholar
|
Find articles by Sun, J. in: PubMed | Google Scholar
Find articles by Gao, B. in: PubMed | Google Scholar
Published August 22, 2025 - More info
JCI Insight. 2025;10(16):e197929. https://doi.org/10.1172/jci.insight.197929.
© 2025 Ma et al. This work is licensed under the Creative Commons Attribution 4.0 International License. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
Related article:
Abstract
Alcohol-associated liver disease is a spectrum of liver disorders with histopathological changes ranging from simple steatosis to steatohepatitis, cirrhosis, and hepatocellular carcinoma. Recent data suggest that chronic-plus-binge ethanol intake induces steatohepatitis by promoting release by hepatocytes of proinflammatory mitochondrial DNA–enriched (mtDNA-enriched) extracellular vesicles (EVs). The aim of the present study was to investigate the role of the stress kinase apoptosis signal–regulating kinase 1 (ASK1) and p38 mitogen-activated protein kinase (p38) in chronic-plus-binge ethanol–induced steatohepatitis and mtDNA-enriched EV release. Microarray analysis revealed the greatest hepatic upregulation of metallothionein 1 and 2 (Mt1/2), which encode 2 of the most potent antioxidant proteins. Genetic deletion of the Mt1 and Mt2 genes aggravated ethanol-induced liver injury, as evidenced by elevation of serum ALT, neutrophil infiltration, oxidative stress, and ASK1/p38 activation in the liver. Inhibition or genetic deletion of Ask1 or p38 ameliorated ethanol-induced liver injury, inflammation, ROS levels, and expression of phagocytic oxidase and ER stress markers in the liver. In addition, inhibition of ASK1 or p38 also attenuated ethanol-induced mtDNA-enriched EV secretion from hepatocytes. Taken together, these findings indicate that induction of hepatic mtDNA-enriched EVs by ethanol is dependent on ASK1 and p38, thereby promoting alcoholic steatohepatitis.
Authors
Jing Ma, Haixia Cao, Robim M. Rodrigues, Mingjiang Xu, Tianyi Ren, Yong He, Seonghwan Hwang, Dechun Feng, Ruixue Ren, Peixin Yang, Suthat Liangpunsakul, Jian Sun, Bin Gao
Original citation: JCI Insight. 2020;5(14):e136496. https://doi.org/10.1172/jci.insight.136496
Citation for this corrigendum: JCI Insight. 2025;10(16):e197929. https://doi.org/10.1172/jci.insight.197929
The authors recently became aware that the GS+E panel in Figure 4B is the same as the LY+E panel in Figure 7B. The error was inadvertent and occurred during the revision process. The correct figure panels are shown below. The HTML and PDF files have been updated.
The authors regret the error.
