Evidence map›Paper›PMID 41596272›Full record

ArticleInternational journal of molecular sciences2026

Vitamin E Modulates Hepatic Extracellular Adenosine Signaling to Attenuate Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD).

Mengting Shan, Magdeline E Carrasco Apolinario, Tomoko Tokumaru, Kenshiro Shikano, Phurpa Phurpa, Ami Kato, Hitoshi Teranishi, Shinichiro Kume, Nobuyuki Shimizu, Tatsuki Kurokawa and 4 more

Abstract read
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In one paragraph

Article in International journal of molecular sciences, 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

14 authors.

Mengting ShanDepartment of Physiology, Faculty of Medicine, Oita University, Yufu 879-5593, Oita, Japan.ORCID 0009-0002-0634-3568
Magdeline E Carrasco ApolinarioDepartment of Physiology, Faculty of Medicine, Oita University, Yufu 879-5593, Oita, Japan.ORCID 0000-0002-4147-0020
Tomoko TokumaruDivision of Gastroenterology, Department of Internal Medicine, Faculty of Medicine, Oita University, Yufu 879-5593, Oita, Japan.ORCID 0000-0001-6343-2618
Kenshiro ShikanoDepartment of Physiology, Faculty of Medicine, Oita University, Yufu 879-5593, Oita, Japan.ORCID 0000-0003-4395-3787
Phurpa PhurpaDepartment of Physiology, Faculty of Medicine, Oita University, Yufu 879-5593, Oita, Japan.
Ami KatoDepartment of Physiology, Faculty of Medicine, Oita University, Yufu 879-5593, Oita, Japan.ORCID 0000-0002-3982-0431
Hitoshi TeranishiDepartment of Physiology, Faculty of Medicine, Oita University, Yufu 879-5593, Oita, Japan.
Shinichiro KumeDepartment of Physiology, Faculty of Medicine, Oita University, Yufu 879-5593, Oita, Japan.
Nobuyuki ShimizuDepartment of Biochemistry and Molecular Genetics, Faculty of Medicine, Oita University, Yufu 879-5593, Oita, Japan.ORCID 0000-0002-8100-0330
Tatsuki KurokawaDepartment of Physiology, Faculty of Medicine, Oita University, Yufu 879-5593, Oita, Japan.
Takatoshi HikidaLaboratory for Advanced Brain Functions, Institute for Protein Research, Osaka University, Suita 565-0871, Osaka, Japan.
Toshikatsu HanadaDepartment of Biochemistry and Molecular Genetics, Faculty of Medicine, Oita University, Yufu 879-5593, Oita, Japan.ORCID 0000-0002-3317-6366
Yulong LiState Key Laboratory of Membrane Biology, School of Life Sciences, Peking University, Beijing 100871, China.
Reiko HanadaDepartment of Physiology, Faculty of Medicine, Oita University, Yufu 879-5593, Oita, Japan.ORCID 0000-0002-7608-1287

Funding

Grant-in-Aid for JSPS Fellows 24KF0066Japan Society for the Promotion of Science (JSPS) KAKENHI 21H03376the Cooperative Research Project Program of the Institute for Protein Research at Osaka University ICR-25-42the Naito Foundation no numberthe Takeda Science Foundation no number
6 · The paper itself

Abstract

Metabolic dysfunction-associated steatotic liver disease (MASLD) involves early disturbances such as excessive lipid accumulation, sterile inflammation, and hepatocellular stress. The results of recent studies have highlighted extracellular ATP and its metabolite adenosine (Ado) as damage-associated molecular patterns (DAMPs) that drive inflammation, endoplasmic reticulum (ER) stress, and steatosis, contributing to MASLD progression. Although vitamin E is clinically used for its antioxidant and anti-inflammatory properties, it remains unclear whether its therapeutic effects involve modulation of DAMP-associated signaling. To address this gap, we used transgenic zebrafish expressing a liver-specific G-protein-coupled receptor activation-based adenosine sensor (GRAB

Indexed as

AdenosineFatty LiverLiverNon-alcoholic Fatty Liver DiseaseSignal TransductionVitamin EAnimalsAnimals, Genetically ModifiedEndoplasmic Reticulum StressSarcoplasmic Reticulum Calcium-Transporting ATPasesZebrafishAdenosineSarcoplasmic Reticulum Calcium-Transporting ATPasesVitamin Eextracellular adenosine (eAdo)GRABAdo sensormetabolic dysfunction-associated steatotic liver disease (MASLD)vitamin Ezebrafish model

Identifiers

PMID41596272
PMCPMC12841576

What Socratic holds

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LicenceCC BY
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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 Socratic graph.