ArticleScience advances2025
Decoding the CHI3L1/IL-13Rα2 signaling nexus in MASH-fibrosis pathogenesis.
Article in Science advances, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- The monoacylglycerol acyltransferase 2 inhibitor VB-85387 reduces MASLD.Journal of lipid research · 2026Article
- Article
- Relationship between different modes of death and premature ovarian insufficiency: a literature review.Apoptosis : an international journal on programmed cell death · 2026Review
- Exercise as a Molecular Therapeutic Tool in MASLD: From Signaling Pathways to Clinical Translation-A Narrative Review.Biomedicines · 2026Review
- Association of Serum Chitinase-3-Like Protein 1 with Liver Fibrosis Severity in Autoimmune Liver Diseases.International journal of general medicine · 2026Article
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Authors and funding
13 authors.
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Abstract
Metabolic dysfunction-associated steatohepatitis (MASH) is a progressive liver disease driven by chronic inflammation and fibrosis, yet the immune mechanisms behind it remain unclear. We identify chitinase 3-like 1 (CHI3L1) as a key mediator linking immune activation to fibrotic remodeling in MASH. Across hepatocyte-macrophage coculture and recombinant interleukin-17A (IL-17A) stimulation assays, we delineate a hepatocyte-associated IL-17A signal that augments macrophage CHI3L1 expression via c-Jun N-terminal kinase (JNK)/c-Jun signaling. CHI3L1 then binds to IL-13Rα2 on hepatic stellate cells (HSCs), triggering a p38 mitogen-activated protein kinase (MAPK)/activating transcription factor 3 (ATF3) cascade that induces lipocalin-2 (LCN2), promoting HSC activation and fibrosis. Using cell-specific knockout models, we show that deleting
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