Semin Liver Dis 2024; 44(03): 319-332
DOI: 10.1055/a-2338-9261
Review Article

Inflammation in Steatotic Liver Diseases: Pathogenesis and Therapeutic Targets

Shengying Qian*
1   Shanghai Institute of Materia Medica (SIMM), Chinese Academy of Sciences, Shanghai, China
2   University of Chinese Academy of Sciences, Beijing, China
,
Xiaolin Wang*
3   Department of Infectious Diseases, Shanghai Jiao Tong University School of Medicine, Ruijin Hospital, Shanghai, China
,
Yingfen Chen
1   Shanghai Institute of Materia Medica (SIMM), Chinese Academy of Sciences, Shanghai, China
2   University of Chinese Academy of Sciences, Beijing, China
,
Qiuhong Zai
1   Shanghai Institute of Materia Medica (SIMM), Chinese Academy of Sciences, Shanghai, China
2   University of Chinese Academy of Sciences, Beijing, China
,
Yong He
1   Shanghai Institute of Materia Medica (SIMM), Chinese Academy of Sciences, Shanghai, China
2   University of Chinese Academy of Sciences, Beijing, China
› Author Affiliations


Preview

Abstract

Alcohol-related liver disease (ALD) and metabolic dysfunction-associated steatotic liver disease (MASLD), two main types of steatotic liver disease (SLDs), are characterized by a wide spectrum of several different liver disorders, including simple steatosis, steatohepatitis, cirrhosis, and hepatocellular carcinoma. Multiple immune cell-mediated inflammatory responses not only orchestrate the killing and removal of infected/damaged cells but also exacerbate the development of SLDs when excessive or persistent inflammation occurs. In recent years, single-cell and spatial transcriptome analyses have revealed the heterogeneity of liver-infiltrated immune cells in ALD and MASLD, revealing a new immunopathological picture of SLDs. In this review, we will emphasize the roles of several key immune cells in the pathogenesis of ALD and MASLD and discuss inflammation-based approaches for effective SLD intervention. In conclusion, the study of immunological mechanisms, especially highly specific immune cell population functions, may provide novel therapeutic opportunities for this life-threatening disease.

Author Contributions

S.Q. wrote inflammation in ALD and therapeutic targets; X.W. wrote inflammation in MASLD; Y.C. prepared [Fig. 1] and [Table 1]; Q.Z. prepared [Fig. 2]; Y.H. initiated and supervised the writing of the entire paper and edited the paper.


* S.Q. and X.W. contributed equally to this work.




Publication History

Accepted Manuscript online:
05 June 2024

Article published online:
25 June 2024

© 2024. Thieme. All rights reserved.

Thieme Medical Publishers, Inc.
333 Seventh Avenue, 18th Floor, New York, NY 10001, USA