ArticleClinical and molecular hepatology2025
GOLM1 promotes cholesterol gallstone formation via ABCG5-mediated cholesterol efflux in metabolic dysfunction-associated steatohepatitis livers.
Article in Clinical and molecular hepatology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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.
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.
Who cites it
11 citing papers in PubMed.
- U-shaped association between dietary flavonoid and gallstone prevalence with sex-specific effects: Insights from a cross-sectional study.The Journal of international medical research · 2026Article
- Anti-Obesity Effects of Pear Extract (International journal of stem cells · 2026Article
- Biliary elimination of cholesterol can be modulated by hepatocyte mitochondrial Aquaporin-8 in mice.Scientific reports · 2026Article
- Integrated multi-omics profiling identifies genetic loci of African swine fever resistance in pigs.GigaScience · 2026Article
- Reply to correspondence 2 on "GOLM1 promotes cholesterol gallstone formation via ABCG5-mediated cholesterol efflux in MASH livers".Clinical and molecular hepatology · 2025Article
- Reply to correspondence 1 on "GOLM1 promotes cholesterol gallstone formation via ABCG5-mediated cholesterol efflux in MASH livers".Clinical and molecular hepatology · 2025Article
- GOLM1 and bile acid synthesis: Correspondence to editorial on "GOLM1 promotes cholesterol gallstone formation via ABCG5-mediated cholesterol efflux in MASH livers".Clinical and molecular hepatology · 2025Article
- Unraveling the role of GOLM1-OPN-ABCG5 axis in MASH: Editorial on "GOLM1 promotes cholesterol gallstone formation via ABCG5-mediated cholesterol efflux in MASH livers".Clinical and molecular hepatology · 2025Article
- Bridging the gap: The GOLM1-OPN-ABCG5 axis in MASH and gallstone disease: Editorial on "GOLM1 promotes cholesterol gallstone formation via ABCG5-mediated cholesterol efflux in MASH livers".Clinical and molecular hepatology · 2025Article
- Correspondence to editorial on "GOLM1 promotes cholesterol gallstone formation via ABCG5-mediated cholesterol efflux in MASH livers".Clinical and molecular hepatology · 2025Article
- Association of arm circumference with the prevalence of gallstones in United States adults: a retrospective analysis on US National Health and Nutrition Examination Survey.Frontiers in medicine · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
Abstract
BACKGROUND/
aimsMetabolic dysfunction-associated steatohepatitis (MASH) is a significant risk factor for gallstone formation, but mechanisms underlying MASH-related gallstone formation remain unclear. Golgi membrane protein 1 (GOLM1) participates in hepatic cholesterol metabolism and is upregulated in MASH. Here, we aimed to explore the role of GOLM1 in MASH-related gallstone formation.
methodsThe UK Biobank cohort was used for etiological analysis. GOLM1 knockout (GOLM1-/-) and wild-type (WT) mice were fed with a high-fat diet (HFD). Livers were excised for histology and immunohistochemistry analysis. Gallbladders were collected to calculate incidence of cholesterol gallstones (CGSs). Biles were collected for biliary lipid analysis. HepG2 cells were used to explore underlying mechanisms. Human liver samples were used for clinical validation.
resultsMASH patients had a greater risk of cholelithiasis. All HFD-fed mice developed MASH, and the incidence of gallstones was 16.7% and 75.0% in GOLM1-/- and WT mice, respectively. GOLM1-/- decreased biliary cholesterol concentration and output. In vivo and in vitro assays confirmed that GOLM1 facilitated cholesterol efflux through upregulating ATP binding cassette transporter subfamily G member 5 (ABCG5). Mechanistically, GOLM1 translocated into nucleus to promote osteopontin (OPN) transcription, thus stimulating ABCG5-mediated cholesterol efflux. Moreover, GOLM1 was upregulated by interleukin-1β (IL-1β) in a dose-dependent manner. Finally, we confirmed that IL-1β, GOLM1, OPN, and ABCG5 were enhanced in livers of MASH patients with CGSs.
conclusionIn MASH livers, upregulation of GOLM1 by IL-1β increases ABCG5-mediated cholesterol efflux in an OPN-dependent manner, promoting CGS formation. GOLM1 has the potential to be a molecular hub interconnecting MASH and CGSs.
Indexed as
Identifiers
What Socratic holds
Registered trials
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.