ArticleInternational journal of biological sciences2026
Hepatic Stellate Cell-derived IL-11 Exacerbates Liver Fibrosis via Interplay between HSCs and Macrophages.
Article in International journal of biological sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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
3 citing papers in PubMed.
- Beyond fibrosis: Emerging role of IL-11 in regulating innate and adaptive immune cell plasticity.Molecular biology reports · 2026Review
- Immune crosstalk in metabolic dysfunction-associated steatotic liver disease: interactions between innate and adaptive immunity.Frontiers in immunology · 2026Review
- The role and therapeutic prospects of intercellular communication and RNA mFrontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It has been a consensus that hepatic microenvironment composed by the non-parenchymal cells networks play a critical role during liver fibrogenesis, with the crosstalk between hepatic stellate cells (HSCs) and macrophages being of paramount importance. Interleukin 11(IL-11) has been implicated as a pro-fibrogenic cytokine, where its function in/between hepatocytes and HSCs has been revealed. But whether IL-11 participates in the interaction of HSCs and macrophages and related mechanism remains obscure. Our research demonstrates that HSC-derived IL-11 operates through a dual mechanism of autocrine activation and paracrine reprogramming to drive the fibrosis. AAV6-mediated IL-11 overexpression in the HSCs aggravated hepatic fibrosis induced by CCl
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