ArticleFrontiers in immunology2025
Type I IFN receptor blockade alleviates liver fibrosis through macrophage-derived STAT3 signaling.
Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Systems biology framework for the rational design of operational conditions for in vitro/in vivo translation of tissue models.Science advances · 2026Article
- Variants ofLife science alliance · 2026Article
- Article
- Persistent IFN-I signaling associated with the HIV-1 reservoir fuels immune exhaustion and reveals therapeutic targets.Frontiers in immunology · 2026Review
- Strategies to promote liver fibrosis amelioration with involvement of restorative macrophages.Frontiers in immunology · 2026Review
- THBS1 as a candidate biomarker and fibrotic mediator in radiation-induced liver injury: insights from TMT-labeled quantitative proteomics.Frontiers in pharmacology · 2025Article
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Authors and funding
4 authors.
Funding
Abstract
Liver macrophages play a role in the development of liver fibrosis progression via the regulation of inflammatory signaling. However, the precise mechanisms of macrophages contributing to liver fibrosis progression remain unclear. Using a preclinical model of CCl4-treated mice, we determined the composition of immune cells and the alteration of inflammatory gene expression. Our findings revealed a significant increase in liver macrophages, particularly those derived from infiltrating blood monocytes, in fibrotic mice. Moreover, the expression levels of type I IFN signature genes such as
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