ArticleCell death & disease2023
The C-type lectin COLEC10 is predominantly produced by hepatic stellate cells and involved in the pathogenesis of liver fibrosis.
Article in Cell death & disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 8 citations in OpenAlex.
- Hepatitis Viruses Infection Up-Regulating Fibrosis Signals in Hepatocellular Carcinoma.Biomedicines · 2026Article
- COLEC10 and COLEC11 are new serum biomarkers of chronic liver disease.European journal of medical research · 2026Article
- Identification of Key Targets of Herbal Compounds for Liver Fibrosis Using Network Pharmacology Combined With Transcriptomics.Gastroenterology research and practice · 2026Article
- Cell-Type Deconvolution Reveals Dynamic Changes in MASLD.Liver international communications · 2025Article
- Article
- [A clinical investigation of constructing a diagnostic model for sepsis-induced coagulopathy utilizing data-independent acquisition proteomics].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2025Article
- Hepatic stellate cell single cell atlas reveals a highly similar activation process across liver disease aetiologies.JHEP reports : innovation in hepatology · 2025Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Hepatic stellate cell is one of the major nonparenchymal cell types in liver. It has been proved the hepatic stellate cells are activated upon liver injury and produce excessive extracellular matrix to induce liver fibrosis. Single-cell RNA sequencing has been introduced to identify the subpopulations and function of hepatic stellate cells for its remarkable resolution of representation of single-cell transcriptome. According to the re-analysis of single-cell RNA sequencing data and pseudotime trajectory inference, we have found the C-type lectins including Colec10 and Colec11 are not produced by hepatocytes but predominantly produced by hepatic stellate cells, especially quiescent ones in the mice livers. In addition, the expression of Colec10 is decreased in the fibrotic livers of CCl4-challenged mice. COLEC10 is also mainly expressed in the hepatic stellate cells of human livers and the expression of COLEC10 is decreased with the progression of liver fibrosis. The bulk RNA sequencing data of the lentivirus transfected LX-2 cells indicates the function of COLEC10 is associated with inflammation, angiogenesis and extracellular matrix alteration. Surprisingly, the in vitro overexpression of COLEC10 in LX-2 cells promotes the mRNA expression of extracellular matrix components including COL1A1, COL1A2 and COL3A1 and the extracellular matrix degradation enzyme MMP2. To further investigate the role of COLEC10 in the pathogenesis of liver fibrosis, the serum concentration of COLEC10 in patients with chronic liver disease and healthy donors is measured. The serum concentration of COLEC10 is elevated in the patients with chronic liver disease compared to the healthy donors and positively correlated with serum concentration of the D-dimer but not the most of liver function markers. Altogether, we conclude that the C-type lectin COLEC10 is predominantly produced by the hepatic stellate cells and involved in the pathogenesis of liver fibrosis.
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