Evidence map›Paper›PMID 38014444›Full record

ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2024

Seladelpar combined with complementary therapies improves fibrosis, inflammation, and liver injury in a mouse model of nonalcoholic steatohepatitis.

Yun-Jung Choi, Jeff D Johnson, Jin-Ju Lee, Jiangao Song, Marcy Matthews, Marc K Hellerstein, Charles A McWherter

Open access · hybridAbstract read
In one paragraph

Article in American journal of physiology. Gastrointestinal and liver physiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

8 citing papers in PubMed, 11 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. The Efficacy and Safety of Seladelpar for Primary Biliary Cholangitis: A Systematic Review and Meta-Analysis.JGH open : an open access journal of gastroenterology and hepatology · 2025
    Review
  6. Review
  7. Review
  8. Review
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

7 authors at 2 institutions in 1 country.

Yun-Jung ChoiCymaBay Therapeutics, Inc., Fremont, California, United States.ORCID 0000-0002-5153-9714
Jeff D JohnsonCymaBay Therapeutics, Inc., Fremont, California, United States.
Jin-Ju LeeCymaBay Therapeutics, Inc., Fremont, California, United States.ORCID 0009-0005-9772-1780
Jiangao SongCymaBay Therapeutics, Inc., Fremont, California, United States.
Marcy MatthewsDepartment of Nutritional Sciences and Toxicology, University of California, Berkeley, Berkeley, California, United States.
Marc K HellersteinDepartment of Nutritional Sciences and Toxicology, University of California, Berkeley, Berkeley, California, United States.
Charles A McWherterCymaBay Therapeutics, Inc., Fremont, California, United States.
CymaBay Therapeutics (United States) · USUniversity of California, Berkeley · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Seladelpar, a selective peroxisome proliferator-activated receptor δ (PPARδ) agonist, improves markers of hepatic injury in human liver diseases, but histological improvement of nonalcoholic steatohepatitis (NASH) and liver fibrosis has been challenging with any single agent. To discover how complementary agents could work with seladelpar to achieve optimal outcomes, this study evaluated a variety of therapeutics (alone and in combination) in a mouse model of NASH. Mice on a high-fat amylin liver NASH (AMLN) diet were treated for 12 wk with seladelpar, GLP-1-R (glucagon-like peptide-1 receptor) agonist liraglutide, apoptosis signal-regulating kinase 1 (ASK1) inhibitor selonsertib, farnesoid X receptor (FXR) agonist obeticholic acid, and with seladelpar in combination with liraglutide or selonsertib. Seladelpar treatment markedly improved plasma markers of liver function. Seladelpar alone or in combination resulted in stark reductions in liver fibrosis (hydroxyproline, new collagen synthesis rate, mRNA indices of fibrosis, and fibrosis staining) compared with vehicle and the other single agents. Robust reductions in liver steatosis were also observed. Seladelpar produced a reorganization of metabolic gene expression, particularly for those genes promoting peroxisomal and mitochondrial lipid oxidation. In summary, substantial improvements in NASH and NASH-induced fibrosis were observed with seladelpar alone and in combination with liraglutide in this model. Broad gene expression analysis suggests seladelpar should be effective in concert with diverse mechanisms of action.

Indexed as

AcetatesBenzamidesComplementary TherapiesImidazolesNon-alcoholic Fatty Liver DiseasePPAR deltaPyridinesAnimalsHumansInflammationLiraglutideLiverLiver CirrhosisMiceMice, Inbred C57BLAcetatesBenzamidesImidazolesLiraglutidePPAR deltaPyridinesseladelparselonsertibcombination therapiesDIO-NASHGLP-1 receptor agonistliver fibrosisPPARδ

Identifiers

PMID38014444
PMCPMC11208022
OpenAlexW4389098143

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.