ArticleCommunications biology2026
TGFBI promotes liver fibrosis through remodeling the profibrotic microenvironment by a positive feedback regulatory loop.
Article in Communications biology, 2026. 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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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.
The trial behind it
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Who cites it
5 citing papers in PubMed.
- Omics data discovery agents: Agent-supported retrieval, reanalysis, and synthesis of published omics data.PLoS computational biology · 2026Article
- A Novel Loss-of-Function Variant inGenes · 2026Article
- Omics Data Discovery Agents: Agent-Supported Retrieval, Reanalysis, and Synthesis of Published Omics Data.ArXiv · 2026Article
- Article
- TGFBI in tumors and the tumor immune microenvironment: functional roles, mechanisms, and therapeutic targeting.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
Liver fibrosis is a major global health burden with limited treatment options. Transforming growth factor-beta-induced protein (TGFBI) is crucial in fibrotic diseases and tumors, however, its precise mechanism in liver fibrosis remains unclear. Here we show that TGFBI promotes liver fibrosis in male C57BL/6 mice. TGFBI is upregulated in fibrotic livers and derived from non-parenchymal cells. Genetic TGFBI deficiency alleviates liver fibrosis in both CCl
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Registered trials
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