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Immunopathogenic mechanisms and immunoregulatory therapies in MASLD
Open accessAbstract
Metabolic dysfunction-associated steatotic liver disease (MASLD), previously known as nonalcoholic fatty liver disease (NAFLD), is the most prevalent chronic liver disease worldwide, with an estimated global prevalence of approximately 30%; however, effective pharmacotherapies are still limited due to its complex pathogenesis and etiology. Therefore, a more thorough understanding of disease pathogenesis is urgently needed. An increasing number of studies suggest that MASLD and its progressive form, metabolic dysfunction-associated steatohepatitis (MASH), are driven by chronic overnutrition, multiple genetic susceptibility factors, and pathogenic consequences, including hepatocyte damage and liver inflammation. Hepatic inflammation is the key event fueling the conversion from simple steatosis to steatohepatitis and fibrosis. Current therapies for MASH, including the recently approved thyroid hormone receptor-beta agonist resmetirom or the available incretin mimetics, mainly target metabolic injury to the liver but not inflammation directly. In this review, we provide an in-depth discussion of current data related to the immunological mechanisms of MASLD and summarize the effects of current and experimental therapies on immunoregulation in MASLD.
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“In addition to competing for survival signals like CSF-1 (9, 33, 34), infiltrating monocytes actively replace embryonic KCs (EmKCs) during injury (35–37).”
From Macrophage duality in liver diseases: heterogeneity, plasticity, and the quest for precision therapeutics (2026) · cites this paper as [37]
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Metadata
- Authors
- He, Y., Chen, Y., Qian, S., van Der Merwe, S., Dhar, D., Brenner, D. A., & Tacke, F.
- Affiliations
- Chinese Academy of Sciences (CN)
- Sanford Burnham Prebys Medical Discovery Institute (US)
- Charité – Universitätsmedizin Berlin (DE)
- Corresponding author
- He, Yong
- Tacke, Frank
- Venue
- Cellular & Molecular Immunology
- Published
- 2025-06-10
- Volume
- 22
- Issue
- 10
- Pages
- 1159-1177
- ISSN
- 1672-7681 (ISSN-L)
- 2042-0226
- PMC
- PMC12480724
- OpenAlex
- W4411162672
- Semantic Scholar
- 7f2f36cf67705164236941f4c20e7acd81779cf2
- Cited by
- 81
- References
- 226
- Citations by year
- 2026: 63 · 2025: 18
- FWCI
- 12.44
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Locations
- Cellular and Molecular Immunology (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed (publishedVersion)
- PubMed Central (publishedVersion, cc-by)
- Lirias (KU Leuven) (submittedVersion, cc-by)
- Funders
- U.S. Department of Health and Human Services (R01DK133930, RO1DK137061)
- Deutsche Forschungsgemeinschaft (SFB 1382, DFGTa434/8‐1, Ta434/8‐1, 403224013)
- National Natural Science Foundation of China (82270601, 403224013)
- National Institutes of Health
- National Key Research and Development Program of China (2024ZD0530604, 2023YFA1800804)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK137061, R01DK133930)
- Topics
- Health Sciences › Medicine › Hepatology › Liver Disease Diagnosis and Treatment
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Health Sciences › Medicine › Hepatology › Liver Diseases and Immunity
- Keywords
- non-alcoholic fatty liver disease, nonalcoholic steatohepatitis, immunopathogenesis, liver inflammation, immunomodulatory therapy, resmetirom, incretin mimetics, liver fibrosis, genetic susceptibility, overnutrition
- MeSH terms
- Animals, Humans, Liver, Immunomodulation, Non-alcoholic Fatty Liver Disease
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