ArticleBMC pediatrics2025
Inflammatory factor CCL2 enhances the interaction between monocyte-macrophage cells and liver parenchymal cells to promote liver inflammation and fibrosis in biliary atresia.
Article in BMC pediatrics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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.
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Who cites it
3 citing papers in PubMed.
- From Mechanisms to Therapeutic Innovation in Non-Small Cell Lung Cancer: A Knowledge-Depth Translational Mapping with Experimental Validation.International journal of molecular sciences · 2026Article
- Biliary atresia-related liver fibrosis.Frontiers in cell and developmental biology · 2026Review
- Conserved Ductular Reaction Mechanisms in Biliary Atresia and Primary Sclerosing Cholangitis Derived From Single-Cell and Spatial Transcriptomics.Cellular and molecular gastroenterology and hepatology · 2026Review
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Authors and funding
12 authors.
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Abstract
backgroundLiver fibrosis in biliary atresia (BA) progresses rapidly and has distinct characteristics; however, current studies have not identified effective prevention or treatment strategies to address this issue.
methodsBA liver tissues with different degrees of liver fibrosis (n = 4), liver tissues of choledochal cyst (n = 2), and liver tissues of the normal control (NC) group (n = 2) were selected. Single-cell RNA sequencing (scRNA-seq), spatial transcriptomics (ST), and Mendelian randomization (MR) were integrated for analysis. The clinical data of the sequenced samples, GSE176189 and GSE122340, were used to verify the results.
resultsThe level of inflammation in the severe fibrosis group was significantly higher than that in the mild fibrosis group (adjusted P < 0.0001). The results of MR showed that CCL2 had a causal relationship with BA (odds ratio (OR) = 1.70, confidence interval (CI): 1.19 to 2.43, P = 0.004, P
conclusionsSevere liver fibrosis in BA is associated with a pronounced inflammatory response. CCL2 may be crucial in the occurrence and progression of liver fibrosis in BA. Targeting CCL2 + monocyte-macrophage cells by reducing their proportion or interaction with liver fibrosis-related cells may provide a potential treatment for liver fibrosis in BA.
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