Evidence map›Paper›PMID 42859620›Full record

ArticleComprehensive physiology2026

Hepatic HIF2α Modulates Extra-Hepatic Disease-Associated Phenotypes During Metabolic Dysfunction-Associated Steatotic Liver Disease.

Lorenz M W Holzner, Rosa M Korpershoek, Youguo Niu, Anna Cochrane, Paula M Darwin, Julia Babuta, Areesha Nazeer, Cecilia Castro, Alice P Sowton, Alice E Knapton and 6 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Comprehensive physiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

16 authors.

Lorenz M W HolznerDepartment of Physiology, Development and Neuroscience University of Cambridge Cambridge UK.ORCID https://orcid.org/0000-0001-8350-2142
Rosa M KorpershoekDepartment of Physiology, Development and Neuroscience University of Cambridge Cambridge UK.
Youguo NiuDepartment of Physiology, Development and Neuroscience University of Cambridge Cambridge UK.
Anna CochraneDepartment of Physiology, Development and Neuroscience University of Cambridge Cambridge UK.ORCID https://orcid.org/0009-0004-7763-7322
Paula M DarwinDepartment of Physiology, Development and Neuroscience University of Cambridge Cambridge UK.ORCID https://orcid.org/0000-0002-8408-4680
Julia BabutaDivision of Systems Medicine, Department of Metabolism, Digestion and Reproduction Imperial College London, Hammersmith Hospital Campus London UK.
Areesha NazeerThe Rowett Institute University of Aberdeen Aberdeen UK.
Cecilia CastroThe Rowett Institute University of Aberdeen Aberdeen UK.
Alice P SowtonDepartment of Physiology, Development and Neuroscience University of Cambridge Cambridge UK.ORCID https://orcid.org/0000-0002-3718-7783
Alice E KnaptonDepartment of Physiology, Development and Neuroscience University of Cambridge Cambridge UK.ORCID https://orcid.org/0000-0002-3512-157X
Benjamin D ThackrayDepartment of Physiology, Development and Neuroscience University of Cambridge Cambridge UK.ORCID https://orcid.org/0000-0002-9171-2454
Julian L GriffinThe Rowett Institute University of Aberdeen Aberdeen UK.
Zoe HallDivision of Systems Medicine, Department of Metabolism, Digestion and Reproduction Imperial College London, Hammersmith Hospital Campus London UK.
Dino A GiussaniDepartment of Physiology, Development and Neuroscience University of Cambridge Cambridge UK.ORCID https://orcid.org/0000-0002-1308-1204
Rob C I WüstDepartment of Human Movement Sciences, Faculty of Behavioural and Movement Sciences Vrije Universiteit Amsterdam, Amsterdam Movement Sciences Amsterdam the Netherlands.ORCID https://orcid.org/0000-0003-3781-5177
Andrew J MurrayDepartment of Physiology, Development and Neuroscience University of Cambridge Cambridge UK.ORCID https://orcid.org/0000-0002-0929-9315

Funding

Wellcome Trust
6 · The paper itself

Abstract

Metabolic dysfunction-associated steatotic liver disease (MASLD) afflicts more than one-third of adults globally, contributing significantly to an increased cardiovascular disease risk. Further, patients with severe liver disease experience muscle weakness and fatigue. Hypoxia-inducible factor 2α (HIF2α) accumulates in the livers of MASLD patients. Here we sought to understand the role of hepatic HIF2α in mediating hepatic and extra-hepatic features of MASLD. Using an obese mouse model of MASLD, we investigated the impact of hepatocyte-specific HIF2α deletion (hHIF2α

Indexed as

cardiac dysfunctionHIF2αhypoxia signalinglipidomicsliverMASLDmetabolismmitochondria

Identifiers

PMID42859620
PMCPMC13652961

What OpenQuestion holds

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Registered trials

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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.