Hepatic Stellate Cell-derived IL-11 Exacerbates Liver Fibrosis via Interplay between HSCs and Macrophages.

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 CCl₄ in C57/B6 mice, accompanied by a

SUBMITTER: Zhang Y 

PROVIDER: S-EPMC12681746 | biostudies-literature | 2026

REPOSITORIES: biostudies-literature