Evidence map›Paper›PMID 40691365›Full record

ArticleNature medicine2025

Modulation of metabolic, inflammatory and fibrotic pathways by semaglutide in metabolic dysfunction-associated steatohepatitis.

Maximilian Jara, Jenny Norlin, Mette Skalshøi Kjær, Kasper Almholt, Kristian M Bendtsen, Elisabetta Bugianesi, Kenneth Cusi, Elisabeth D Galsgaard, Milan Geybels, Lise L Gluud and 11 more

Abstract read
In one paragraph

Article in Nature medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed, 3 pooled it
–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

53 citing papers in PubMed, 3 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Review
  5. Review
  6. Article
  7. Selecting Pharmacologic Interventions for MASH.Digestive diseases and sciences · 2026
    Review
  8. Review
  9. Review
  10. Review
  11. Review
  12. Review
  13. Review
  14. Autophagy in MASLD: A Metabolic and Precision Medicine Perspective.Liver international : official journal of the International Association for the Study of the Liver · 2026
    Review
  15. Article
  16. Article
  17. Review
  18. Review
  19. The evolving landscape of obesity pharmacotherapy.Nature reviews. Drug discovery · 2026
    Review
  20. DGAT2 inhibition in MASH: histologic promise and lipid paradox.Hepatobiliary surgery and nutrition · 2026
    Article
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

21 authors.

Maximilian Jara *Novo Nordisk, Clinical Development, Søborg, Denmark.
Jenny Norlin *Novo Nordisk, Research & Early Development, Måløv, Denmark.ORCID http://orcid.org/0000-0002-4825-6975
Mette Skalshøi Kjær *Novo Nordisk, Clinical Development, Søborg, Denmark.ORCID http://orcid.org/0000-0001-6322-4077
Kasper AlmholtNovo Nordisk, Research & Early Development, Måløv, Denmark.ORCID http://orcid.org/0000-0002-9250-514X
Kristian M BendtsenNovo Nordisk, Research & Early Development, Måløv, Denmark.
Elisabetta BugianesiDivision of Gastroenterology, Department of Medical Sciences, University of Torino, Torino, Italy.
Kenneth CusiDivision of Endocrinology, Diabetes, and Metabolism, University of Florida, Gainesville, FL, USA.
Elisabeth D GalsgaardNovo Nordisk, Research & Early Development, Måløv, Denmark.
Milan GeybelsNovo Nordisk, Data Science, Søborg, Denmark.
Lise L GluudGastro Unit, Copenhagen University Hospital Hvidovre, Hvidovre, Denmark and Department of Medicine, University of Copenhagen, Copenhagen, Denmark.ORCID http://orcid.org/0000-0002-9462-4468
Lea M HarderNovo Nordisk, Research & Early Development, Måløv, Denmark.ORCID http://orcid.org/0009-0007-6126-3380
Rohit LoombaRadcliffe Department of Medicine, Oxford University, Oxford, UK.
Gianluca MazzoniNovo Nordisk, Research & Early Development, Måløv, Denmark.ORCID http://orcid.org/0000-0003-2397-1064
Philip N NewsomeRoger Williams Institute of Liver Studies, School of Immunobiology and Microbial Sciences, Faculty of Life Sciences & Medicine, King's College London and King's College Hospital, London, UK.
Louise M NitzeNovo Nordisk, Clinical Development, Søborg, Denmark.
Mads S PalleNovo Nordisk, Data Science, Søborg, Denmark.
Vlad RatziuSorbonne University, ICAN - Institute for Cardiometabolism and Nutrition, Hôpital Pitié Salpêtrière, Paris, France.ORCID http://orcid.org/0000-0002-6865-3791
Anne-Sophie SejlingNovo Nordisk, Clinical Development, Søborg, Denmark.
Vincent W-S WongDepartment of Medicine and Therapeutics, The Chinese University of Hong Kong, Hong Kong, China.ORCID http://orcid.org/0000-0003-2215-9410
Quentin M AnsteeTranslational & Clinical Research Institute, Faculty of Medical Sciences, Newcastle University, Newcastle upon Tyne, UK.ORCID http://orcid.org/0000-0002-9518-0088
Lotte B KnudsenNovo Nordisk, Research & Early Development, Måløv, Denmark. lbkn@novonordisk.com.ORCID http://orcid.org/0000-0002-2439-7116

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metabolic dysfunction-associated steatohepatitis (MASH) is a chronic liver disease strongly associated with cardiometabolic risk factors. Semaglutide, a glucagon-like peptide-1 receptor agonist, improves liver histology in MASH, but the underlying signals and pathways driving semaglutide-induced MASH resolution are not well understood. Here we show that, in two preclinical MASH models, semaglutide improved histological markers of fibrosis and inflammation and reduced hepatic expression of fibrosis-related and inflammation-related gene pathways. Aptamer-based proteomic analyses of serum samples from patients with MASH in a clinical trial identified 72 proteins significantly associated with MASH resolution and semaglutide treatment, with most related to metabolism and several implicated in fibrosis and inflammation. An independent real-world cohort verified the pathophysiological relevance of this signature, showing that the same 72 proteins are differentially expressed in patients with MASH relative to healthy individuals. Taken together, these data suggest that semaglutide may revert the circulating proteome associated with MASH to the proteomic pattern observed in healthy individuals.

Indexed as

Fatty LiverGlucagon-Like PeptidesInflammationLiver CirrhosisAnimalsFemaleGlucagon-Like Peptide 1HumansLiverMaleMiceMiddle AgedProteomicsSemaglutideGlucagon-Like Peptide 1Glucagon-Like PeptidesSemaglutide

Identifiers

PMID40691365
PMCPMC12443624

What OpenQuestion holds

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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.