Evidence map›Paper›PMID 42043860›Full record

ArticleHepatology communications2026

Lumican-TLR4 interaction accelerates hepatic fibrosis by activating hepatic stellate cells.

Yongqiang Xiong, Huanhuan Zhang, Ao Wang, Yaqian Cui, Jiaxi Ye, Leiming Jin, Mengsha Lin, Qianhui Zhang, Guang Liang, Wu Luo and 2 more

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Article in Hepatology communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

12 authors.

Yongqiang XiongDepartment of Endocrine and Metabolic Diseases, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China.
Huanhuan ZhangDepartment of Gastroenterology, Shaanxi Second Provincial People's Hospital, Xi'an, Shaanxi, China.
Ao WangChemical Biology Research Center, Wenzhou Medical University, Wenzhou, Zhejiang, China.
Yaqian CuiChemical Biology Research Center, Wenzhou Medical University, Wenzhou, Zhejiang, China.
Jiaxi YeChemical Biology Research Center, Wenzhou Medical University, Wenzhou, Zhejiang, China.
Leiming JinChemical Biology Research Center, Wenzhou Medical University, Wenzhou, Zhejiang, China.
Mengsha LinChemical Biology Research Center, Wenzhou Medical University, Wenzhou, Zhejiang, China.
Qianhui ZhangChemical Biology Research Center, Wenzhou Medical University, Wenzhou, Zhejiang, China.
Guang LiangSchool of Pharmaceutical Sciences, Hangzhou Medical College, Hangzhou, Zhejiang, China.
Wu LuoChemical Biology Research Center, Wenzhou Medical University, Wenzhou, Zhejiang, China.
Weiwei ZhuChemical Biology Research Center, Wenzhou Medical University, Wenzhou, Zhejiang, China.
Xiang HuDepartment of Endocrine and Metabolic Diseases, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLumican expression is associated with liver fibrosis across various etiologies. However, its precise role and underlying mechanisms in liver fibrosis remain unclear.

methodsLumican knockout (Lum KO) mice were generated, and liver fibrosis was induced using bile duct ligation (BDL) and carbon tetrachloride (CCl4) to investigate the in vivo role of Lumican. Proteomic analyses and target validation were performed to elucidate the mechanisms by which Lumican contributes to liver fibrosis.

resultsLumican is predominantly expressed in hepatic stellate cells (HSCs) and promotes their activation. Lumican deficiency attenuates liver fibrosis progression in mice following BDL and CCl4 administration. Proteomic analysis identified Lumican as a ligand of toll-like receptor 4 (TLR4). Lumican directly binds to TLR4, activating downstream SMAD3-mediated pro-fibrotic signaling pathways, thereby promoting HSC activation and contributing to liver fibrosis development.

conclusionsLumican plays a critical role in HSC activation and liver fibrosis progression via the Lumican-TLR4-SMAD3 axis, highlighting it as a potential therapeutic target for anti-fibrotic intervention.

Indexed as

Hepatic Stellate CellsLiver CirrhosisLumicanToll-Like Receptor 4AnimalsCarbon TetrachlorideMaleMiceMice, KnockoutSignal TransductionSmad3 ProteinCarbon TetrachlorideLumicanLum protein, mouseSmad3 ProteinSmad3 protein, mouseTlr4 protein, mouseToll-Like Receptor 4BDLliver fibrosisSMAD3TLR4

Identifiers

PMID42043860
PMCPMC13120511

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