Evidence map›Paper›PMID 41675316›Full record

ArticleTranslational gastroenterology and hepatology2026

Leptin-dependent fat accumulation triggers autophagy in metabolic dysfunction-associated steatohepatitis model.

Sophia C H Polte, Tomomitsu Matono, Kinya Okamoto, Masahiko Koda, Ali Ebrahimifard, Michael Wanzel, Thorsten Stiewe, Thaddeus T Wissniowski, Sami Matrood, Pietro Di Fazio

Abstract read
In one paragraph

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

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1 · What the graph read from it

What it found

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2 · The registry

The trial behind it

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3 · Its place in the literature

Who cites it

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4 · The record

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5 · Who and what money

Authors and funding

10 authors.

Sophia C H PoltePsychiatry and Psychotherapy, Ernst von Bergmann Clinic Potsdam, Potsdam, Germany.
Tomomitsu MatonoSecond Department of Internal Medicine, Tottori University, Yonago, Tottori, Japan.
Kinya OkamotoSecond Department of Internal Medicine, Tottori University, Yonago, Tottori, Japan.
Masahiko KodaSecond Department of Internal Medicine, Tottori University, Yonago, Tottori, Japan.
Ali EbrahimifardDepartment of Nuclear Medicine, Philipps University Marburg, Marburg, Germany.
Michael WanzelInstitute of Molecular Oncology, Philipps University Marburg, Marburg, Germany.
Thorsten StieweInstitute of Molecular Oncology, Philipps University Marburg, Marburg, Germany.
Thaddeus T WissniowskiCenter for Internal Medicine II, Chemnitz Hospital gGmbH, Chemnitz, Germany.
Sami MatroodInstitute for Radiology, University Hospital Düsseldorf, Düsseldorf, Germany.
Pietro Di FazioDepartment of Nuclear Medicine, Philipps University Marburg, Marburg, Germany.ORCID https://orcid.org/0000-0003-0091-8498

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Metabolic dysfunction-associated steatotic liver disease (MASLD) is a metabolic syndrome characterized by increased fat storage in hepatocytes. In the hepatocytes, autophagy protects against cytotoxic stress and harmful cellular conditions. In the hepatic stellate cells (HSCs), autophagy exerts pro-fibrotic properties and promotes the release of pro-inflammatory metabolites. We investigated the modulation of autophagy as a therapeutic approach for MASLD. Methods: Murine liver tissue and human hepatic cells were analyzed by reverse transcription quantitative polymerase chain reaction (RT-qPCR) and Western blot. Real time fluorescence was performed to monitor the autophagy maturation process. Accumulation of fat was detected by Oil Red O staining. Collagen fibers were detected by picrosirius staining under polarized light. Results: The loss of leptin in obese mice affected by metabolic dysfunction-associated steatohepatitis (MASH) promoted the over-expression of Conclusions: Leptin loss contributes to the autophagy process in obese mice. The administration of oleic acid in

Indexed as

Autophagyleptinmetabolic dysfunction-associated steatohepatitis (MASH)metabolic dysfunction-associated steatotic liver disease (MASLD)metabolism

Identifiers

PMID41675316
PMCPMC12887277

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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.