Evidence map›Paper›PMID 35031697›Full record

ArticleInternational journal of obesity (2005)2022

Adipocyte GPX4 protects against inflammation, hepatic insulin resistance and metabolic dysregulation.

Julian Schwärzler, Lisa Mayr, Bernhard Radlinger, Felix Grabherr, Maureen Philipp, Bernhard Texler, Christoph Grander, Andreas Ritsch, Monika Hunjadi, Barbara Enrich and 6 more

Abstract read
PubMed Publisher
In one paragraph

Article in International journal of obesity (2005), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.7field-weighted citation impact, top 9% of its field
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

26 citing papers in PubMed, 35 citations in OpenAlex.

  1. Review
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  8. Unlocking the Neuroprotective Potential ofAntioxidants (Basel, Switzerland) · 2026
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  11. Article
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  15. Molecular mechanisms of ferroptosis in cardiovascular disease.Molecular and cellular biochemistry · 2024
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  16. Review
  17. Article
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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 at 2 institutions in 2 countries.

Julian Schwärzler *Department of Internal Medicine I, Gastroenterology, Hepatology & Endocrinology, Medical University of Innsbruck, Innsbruck, Austria.
Lisa Mayr *Department of Internal Medicine I, Gastroenterology, Hepatology & Endocrinology, Medical University of Innsbruck, Innsbruck, Austria.
Bernhard RadlingerDepartment of Internal Medicine I, Gastroenterology, Hepatology & Endocrinology, Medical University of Innsbruck, Innsbruck, Austria.
Felix GrabherrDepartment of Internal Medicine I, Gastroenterology, Hepatology & Endocrinology, Medical University of Innsbruck, Innsbruck, Austria.
Maureen PhilippDepartment of Internal Medicine I, Gastroenterology, Hepatology & Endocrinology, Medical University of Innsbruck, Innsbruck, Austria.
Bernhard TexlerDepartment of Internal Medicine I, Gastroenterology, Hepatology & Endocrinology, Medical University of Innsbruck, Innsbruck, Austria.
Christoph GranderDepartment of Internal Medicine I, Gastroenterology, Hepatology & Endocrinology, Medical University of Innsbruck, Innsbruck, Austria.
Andreas RitschDepartment of Internal Medicine I, Gastroenterology, Hepatology & Endocrinology, Medical University of Innsbruck, Innsbruck, Austria.
Monika HunjadiDepartment of Internal Medicine I, Gastroenterology, Hepatology & Endocrinology, Medical University of Innsbruck, Innsbruck, Austria.
Barbara EnrichDepartment of Internal Medicine I, Gastroenterology, Hepatology & Endocrinology, Medical University of Innsbruck, Innsbruck, Austria.
Karin SalzmannDepartment of Internal Medicine I, Gastroenterology, Hepatology & Endocrinology, Medical University of Innsbruck, Innsbruck, Austria.
Qitao RanDepartment of Cell Systems and Anatomy, UT Health San Antonio, San Antonio, TX, USA.
Lukas A HuberInstitute of Cell Biology, Biocenter, Medical University of Innsbruck, Innsbruck, Austria.
Herbert TilgDepartment of Internal Medicine I, Gastroenterology, Hepatology & Endocrinology, Medical University of Innsbruck, Innsbruck, Austria.ORCID http://orcid.org/0000-0002-4235-2579
Susanne Kaser *Department of Internal Medicine I, Gastroenterology, Hepatology & Endocrinology, Medical University of Innsbruck, Innsbruck, Austria.
Timon E Adolph *Department of Internal Medicine I, Gastroenterology, Hepatology & Endocrinology, Medical University of Innsbruck, Innsbruck, Austria. timon-erik.adolph@i-med.ac.at.ORCID http://orcid.org/0000-0002-4736-830X
Innsbruck Medical University · ATThe University of Texas Health Science Center at San Antonio · US

Funding

Austrian Science Fund FWF P 29379Austrian Science Fund FWF P 33070
6 · The paper itself

Abstract

objectivesMetabolic inflammation is a hallmark of obesity and related disorders, afflicting substantial morbidity and mortality to individuals worldwide. White visceral and subcutaneous adipose tissue not only serves as energy storage but also controls metabolism. Adipose tissue inflammation, commonly observed in human obesity, is considered a critical driver of metabolic perturbation while molecular hubs are poorly explored. Metabolic stress evoked by e.g. long-chain fatty acids leads to oxidative perturbation of adipocytes and production of inflammatory cytokines, fuelling macrophage infiltration and systemic low-grade inflammation. Glutathione peroxidase 4 (GPX4) protects against lipid peroxidation, accumulation of oxygen-specific epitopes and cell death, collectively referred to as ferroptosis. Here, we explore the function of adipocyte GPX4 in mammalian metabolism.

methodsWe studied the regulation and function of GPX4 in differentiated mouse adipocytes derived from 3T3-L1 fibroblasts. We generated two conditional adipocyte-specific Gpx4 knockout mice by crossing Gpx4

resultsGPX4 expression was induced during and required for adipocyte differentiation. In mature adipocytes, impaired GPX4 activity spontaneously evoked lipid peroxidation and expression of inflammatory cytokines such as TNF-α, interleukin 1β (IL-1β), IL-6 and the IL-8 homologue CXCL1. Gpx4

conclusionAdipocyte GPX4 protects against spontaneous metabolic dysregulation and systemic low-grade inflammation independent from ferroptosis, which could be therapeutically exploited in the future.

Indexed as

Insulin ResistanceAdipocytesAdipose TissueAnimalsCytokinesDiet, High-FatEpitopesInflammationMammalsMiceMice, Inbred C57BLMice, KnockoutObesityOxygenPhospholipid Hydroperoxide Glutathione PeroxidaseCytokinesEpitopesglutathione peroxidase 4, mouseOxygenPhospholipid Hydroperoxide Glutathione Peroxidase

Identifiers

PMID35031697
OpenAlexW4206138586

What OpenQuestion holds

Textmetadata
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.