ArticleJournal of gastroenterology2025
Association between advanced fibrosis and epigenetic age acceleration among individuals with MASLD.
Article in Journal of gastroenterology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Associations of Accelerated DNA Methylation Aging Algorithms with Chronic Liver Disease and All-Cause Mortality.Biomedicines · 2026Article
- Fibrosis and Perinatal Features Correlated with Telomere Shortening in Pediatric Metabolic Dysfunction-Associated Steatotic Liver Disease.Life (Basel, Switzerland) · 2026Article
- Pilot study of epigenetic aging and treatment response to semaglutide in the SLIM LIVER study.npj aging · 2026Article
- Low anti-Mullerian hormone in reproductive age is associated with MASLD in midlife.Hepatology communications · 2026Article
- Epigenetic Aging and Treatment Response to Semaglutide in the SLIM LIVER Study.Research square · 2025Article
- Gradual DNA methylation changes reveal transcription factors implicated in metabolic dysfunction-associated steatotic liver disease progression and epigenetic age acceleration.Clinical epigenetics · 2025Article
- Association Between Active DNA Demethylation and Liver Fibrosis in Individuals with Metabolic-Associated Steatotic Liver Disease (MASLD).International journal of molecular sciences · 2025Article
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Authors and funding
10 authors.
Funding
Abstract
backgroundThe biological process of aging plays an important role in the progress of liver fibrosis. However, epidemiological evidence about the associations between advanced fibrosis and epigenetic age acceleration (EAA) among individuals with metabolic dysfunction-associated steatotic liver disease (MASLD) is limited.
methodsWe utilized publicly available DNA methylation data (GSE180474) for our analysis. Five EAA measures were calculated in this study, including IEAA, PhenoAA, GrimAA, DunedinPACE, and DNAmTLAA. Separate linear regression models were conducted to explore the associations between different fibrosis grades and each measure of EAA.
resultsA total of 325 participants were included in this study, with a mean (± SD) age of 48.56 ± 11.50 years. Of these participants, 64.6% with no fibrosis, 16.9% with bridging fibrosis, 11.1% with incomplete cirrhosis, and 7.4% with cirrhosis. After adjusting for demographics and medication status, MASLD individuals with advanced fibrosis were associated with a 5% increase in the pace of aging (DunedinPACE, β = 0.05, 95% CI: 0.03-0.07) and a 10% decrease in DNAmTLAA (β = -0.10, 95% CI: -0.13 to -0.07) compared those without fibrosis. Similarly, higher stages of fibrosis were associated with an increased pace of aging (DunedinPACE, β = 0.02, 95% CI: 0.01-0.03, P
conclusionsOur findings suggest that advanced fibrosis was associated with an accelerated pace of aging, as measured by the third-generation EA measure DunedinPACE, and shorter telomere length, captured by DNAmTLAA, among individuals with MASLD. This finding has potential prognostic implications and suggests EAA may serve as a surrogate marker of therapeutic efficacy in MASLD.
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