ArticleBMC gastroenterology2025
BIGH3 as a potential biomarker for fibrosis in metabolic dysfunction-associated steatotic liver disease: insights from mouse and human studies.
Article in BMC gastroenterology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundLiver fibrosis is the strongest predictor of long-term clinical outcomes in patients with metabolic dysfunction-associated steatotic liver disease MASLD. Non-invasive methods for identifying these patients are urgently needed. We aimed to investigate the link between the transforming growth factor-β induced protein Ig-H3 (BIGH3) and fibrosis in both diet-induced mouse model and patients with MASLD, and explore its potential use as a biomarker for MASLD related fibrosis.
methodsHepatic gene expression and serum BIGH3 levels were studied in two diet -induced MASLD models. Forty patients with biopsy-proven MASLD were recruited. Serum BIGH3 levels were measured by enzyme-linked immunosorbent assays. The difference between groups with or without fibrosis was analyzed using the Mann-Whitney U test. BIGH3 levels across different fibrosis stages were analyzed using Spearman correlation, Kruskal-Wallis test, and Dunn's post-hoc test. The receiver operating characteristic (ROC) curve was used to explore its value in the diagnosis of MASLD related fibrosis.
resultsBigh3 was identified as a fibrosis-related gene in the liver. Serum BIGH3 levels were significantly higher in the mouse model of fibrosis than in controls (P < 0.01). Additionally, serum BIGH3 levels were significantly elevated in MASLD patients with fibrosis compared to those without fibrosis (P < 0.01), and showed a stepwise increase corresponding to the degree of fibrosis (ρ = 0.55, P < 0.01). The areas under the receiver operating characteristic curve to discriminate significant fibrosis were 0.790 (P < 0.01).
conclusionBIGH3 is a potential non-invasive biomarker of MASLD related fibrosis. It may be beneficial for diagnosing significant fibrosis in MASLD patients.
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