Evidence map›Paper›PMID 42737510›Full record

ArticleInternational journal of molecular sciences2026

Selective PPARα Modulator Pemafibrate Ameliorates Metabolic Dysfunction-Associated Steatotic Liver Disease Through Regulation of Leptin Signaling and Remodeling of Gut Microbiota.

Koji Yamamoto, Masaru Baba, Akinori Kubo, Ren Yamada, Akihisa Nakamura, Kenichi Morikawa, Masatsugu Ohara, Masato Nakai, Takuya Sho, Goki Suda and 3 more

Abstract read
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

13 authors.

Koji YamamotoDepartment of Gastroenterology and Hepatology, Hokkaido University Faculty of Medicine and Graduate School of Medicine, Sapporo 060-8648, Japan.
Masaru BabaDepartment of Gastroenterology, JCHO Hokkaido Hospital, Sapporo 062-8618, Japan.
Akinori KuboDepartment of Gastroenterology and Hepatology, Hokkaido University Faculty of Medicine and Graduate School of Medicine, Sapporo 060-8648, Japan.
Ren YamadaDepartment of Gastroenterology and Hepatology, Hokkaido University Faculty of Medicine and Graduate School of Medicine, Sapporo 060-8648, Japan.
Akihisa NakamuraDepartment of Gastroenterology and Hepatology, Hokkaido University Faculty of Medicine and Graduate School of Medicine, Sapporo 060-8648, Japan.
Kenichi MorikawaDepartment of Gastroenterology and Hepatology, Hokkaido University Faculty of Medicine and Graduate School of Medicine, Sapporo 060-8648, Japan.ORCID 0000-0002-3891-5113
Masatsugu OharaDepartment of Gastroenterology and Hepatology, Hokkaido University Faculty of Medicine and Graduate School of Medicine, Sapporo 060-8648, Japan.
Masato NakaiDepartment of Gastroenterology and Hepatology, Hokkaido University Faculty of Medicine and Graduate School of Medicine, Sapporo 060-8648, Japan.
Takuya ShoDepartment of Gastroenterology and Hepatology, Hokkaido University Faculty of Medicine and Graduate School of Medicine, Sapporo 060-8648, Japan.
Goki SudaDepartment of Gastroenterology and Hepatology, Hokkaido University Faculty of Medicine and Graduate School of Medicine, Sapporo 060-8648, Japan.
Koji OgawaDepartment of Gastroenterology and Hepatology, Hokkaido University Faculty of Medicine and Graduate School of Medicine, Sapporo 060-8648, Japan.
Ken FuruyaDepartment of Gastroenterology, JCHO Hokkaido Hospital, Sapporo 062-8618, Japan.
Naoya SakamotoDepartment of Gastroenterology and Hepatology, Hokkaido University Faculty of Medicine and Graduate School of Medicine, Sapporo 060-8648, Japan.ORCID 0000-0003-0061-059X

Funding

Japan Agency for Medical Research and Development JP20fk0210053Japan Agency for Medical Research and Development JP20fk0210056Japan Agency for Medical Research and Development JP20fk0210067Japan Agency for Medical Research and Development JP20fk0210072Japan Agency for Medical Research and Development JP20fk0310101Japan Agency for Medical Research and Development JP20fk0310103Japan Society for the Promotion of Science JP19K18956Japan Society for the Promotion of Science JP20K08371Japan Society for the Promotion of Science JP25K14859
6 · The paper itself

Abstract

Metabolic dysfunction-associated steatotic liver disease (MASLD) is one of the leading causes of chronic liver disease worldwide, and effective pharmacological therapies remain limited. Pemafibrate (Pema), a selective peroxisome proliferator-activated receptor alpha (PPARα) modulator (SPPARMα), has shown promising therapeutic potential in patients with MASLD and hypertriglyceridemia; however, its underlying mechanisms remain incompletely understood. Here, we investigated the therapeutic effects and molecular mechanisms of Pema using in vitro and in vivo MASLD models and evaluated its clinical relevance in patients with MASLD. In a choline-deficient, L-amino acid-defined, high-fat diet (CDAHFD)-induced MASLD mouse model, Pema dose-dependently ameliorated hepatic steatosis and fibrosis and significantly suppressed the hepatic expression of inflammatory and fibrogenic genes, including TLR4, TNFα, αSMA, and Col1A1. Pema also favorably altered the gut microbiota by increasing the abundance of the phylum

Indexed as

BenzoxazolesButyratesFatty LiverGastrointestinal MicrobiomeLeptinPPAR alpha3T3-L1 CellsAnimalsDiet, High-FatDisease Models, AnimalHumansLiverMaleMiceMice, Inbred C57BLSignal TransductionBenzoxazolesButyratesLeptinPPAR alpha(R)-2-(3-((benzoxazol-2-yl-d4 (3-(4-methoxyphenoxy-d7)propyl)amino)methyl)phenoxy) butanoic acidgut–liver axisgut microbiotaleptinMASLDpemafibrate

Identifiers

PMID42737510
PMCPMC13566180

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.