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Novel insights into macrophage immunometabolism in nonalcoholic steatohepatitis.

Authors :
Yuan, Yali
Zhang, Ye
Lu, Xinyu
Li, Junxiang
Wang, Muyuan
Zhang, Wenji
Zheng, Mengyu
Sun, Zhongmei
Xing, Yunqi
Li, Yitong
Qu, Yingdi
Jiao, Yao
Han, Haixiao
Xie, Chune
Mao, Tangyou
Source :
International Immunopharmacology. Apr2024, Vol. 131, pN.PAG-N.PAG. 1p.
Publication Year :
2024

Abstract

• This manuscript summarizes the role of macrophage immunometabolism in NASH, especially the function conversion. • The progress of regulatory factors of macrophage immunometabolism in NASH has been updated. Targeting macrophage immunometabolism become a potential strategy for treating NASH. Nonalcoholic steatohepatitis (NASH), an inflammatory subtype of nonalcoholic fatty liver disease (NAFLD), is characterized by liver steatosis, inflammation, hepatocellular injury and different degrees of fibrosis, and has been becoming the leading cause of liver-related morbidity and mortality worldwide. Unfortunately, the pathogenesis of NASH has not been completely clarified, and there are no approved therapeutic drugs. Recent accumulated evidences have revealed the involvement of macrophage in the regulation of host liver steatosis, inflammation and fibrosis, and different phenotypes of macrophages have different metabolic characteristics. Therefore, targeted regulation of macrophage immunometabolism may contribute to the treatment and prognosis of NASH. In this review, we summarized the current evidences of the role of macrophage immunometabolism in NASH, especially focused on the related function conversion, as well as the strategies to promote its polarization balance in the liver, and hold promise for macrophage immunometabolism-targeted therapies in the treatment of NASH. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
15675769
Volume :
131
Database :
Academic Search Index
Journal :
International Immunopharmacology
Publication Type :
Academic Journal
Accession number :
176432727
Full Text :
https://doi.org/10.1016/j.intimp.2024.111833