ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026
Autocrine Netrin-1 Signaling in Hepatic Stellate Cells Drives Liver Fibrosis and Diet-Induced Metabolic Dysfunction-Associated Steatohepatitis in Mice.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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.
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Who cites it
4 citing papers in PubMed.
- OAF Blocks SIAH1-Mediated Degradation of SCPX, a Therapeutic Strategy for MASLD.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Review
- Autocrine Netrin-1 Signaling in Hepatic Stellate Cells Drives Liver Fibrosis and Diet-Induced Metabolic Dysfunction-Associated Steatohepatitis in Mice.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Calcium imbalance drives organelle network collapse and immune remodeling: novel pathogenic mechanisms in MASLD progression.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Liver fibrosis is a central feature of progressive liver diseases, including metabolic dysfunction-associated steatohepatitis (MASH). The profibrotic liver microenvironment drives hepatic stellate cell (HSC) activation and collagen deposition. However, the nature of HSC-mediated autocrine signaling during the fibrotic response has not been completely characterized. Here, we identify Netrin-1 as an autocrine factor that drives HSC activation and liver fibrosis in patients with MASH. Hepatic Netrin-1 expression was consistently elevated across multiple experimental models of liver fibrosis. Functional studies showed that adenovirus-associated virus (AAV)-mediated hepatic Netrin-1 overexpression exacerbated fibrosis, whereas HSC-specific conditional ablation of Netrin-1 markedly attenuated diet-induced MASH and CCl4-induced liver fibrosis. Notably, lipid nanoparticle-mediated siRNA knockdown of Netrin-1 ameliorated liver fibrosis in mice. Mechanistic investigations revealed that Netrin-1 promotes HSC activation through autocrine signaling mediated by the UNC5B receptor, which triggers rapid intracellular Ca
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Registered trials
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