Evidence map›Paper›PMID 40494889›Full record

ReviewCellular & molecular immunology2025

Immunopathogenic mechanisms and immunoregulatory therapies in MASLD.

Yong He, Yingfen Chen, Shengying Qian, Schalk van Der Merwe, Debanjan Dhar, David A Brenner, Frank Tacke

Abstract readReview
In one paragraph

Review in Cellular & molecular immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

56 citing papers in PubMed.

  1. From Single Agents to Synergy: Redefining Therapeutic Strategies in MASLD.International journal of molecular sciences · 2026
    Review
  2. Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Review
  13. Observational
  14. Article
  15. Review
  16. Review
  17. Review
  18. Article
  19. Article
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Yong He *State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica (SIMM), Chinese Academy of Sciences, Shanghai, China. heyong@simm.ac.cn.ORCID 0009-0006-8681-5287
Yingfen Chen *State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica (SIMM), Chinese Academy of Sciences, Shanghai, China.
Shengying QianState Key Laboratory of Drug Research, Shanghai Institute of Materia Medica (SIMM), Chinese Academy of Sciences, Shanghai, China.
Schalk van Der MerweLaboratory of Hepatology, CHROMETA Department, KU Leuven, Leuven, Belgium.
Debanjan DharDepartment of Medicine, School of Medicine, University of California, San Diego, CA, USA.
David A BrennerDepartment of Medicine, School of Medicine, University of California, San Diego, CA, USA.
Frank TackeDepartment of Hepatology & Gastroenterology, Charité-Universitätsmedizin Berlin, Campus Virchow-Klinikum and Campus Charité Mitte, Berlin, Germany. frank.tacke@charite.de.ORCID 0000-0001-6206-0226

Funding

Dissecting the Intracellular and Extracellular Role of TREM2 in the Pathogenesis of Non-Alcoholic Steatohepatitis.R01DK137061 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Debanjan Dhar · 2023 to 2026
$2.6M
Ubiquitin D as a potential therapeutic target for NASH, HCC and chronic kidney diseasesR01DK133930 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Debanjan Dhar · 2023 to 2026
$2.0M
Deutsche Forschungsgemeinschaft (German Research Foundation) DFG Ta434/8-1Deutsche Forschungsgemeinschaft (German Research Foundation) SFB1382National Natural Science Foundation of China (National Science Foundation of China) 82270601NIDDK NIH HHS R01 DK133930NIDDK NIH HHS R01 DK137061U.S. Department of Health & Human Services | National Institutes of Health (NIH) R01DK133930U.S. Department of Health & Human Services | National Institutes of Health (NIH) RO1DK137061
6 · The paper itself

Abstract

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.

Indexed as

ImmunomodulationNon-alcoholic Fatty Liver DiseaseAnimalsHumansLiverinflammationMASHMASLDpathogenesis.

Identifiers

PMID40494889
PMCPMC12480724

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.