ArticleParasites & vectors2026
Blockade of the CCL2-CCR2 axis attenuates fibrosis and parasite load in vesicular echinococcosis by inhibiting the PI3K-AKT pathway that regulates angiogenesis and hepatic stellate cell apoptosis.
Article in Parasites & vectors, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 1 paper.
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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
1 citing paper in PubMed.
Corrections and comments
- Erratum issued
Authors and funding
10 authors.
Funding
Abstract
backgroundThe C-C motif chemokine ligand 2 (CCL2)-C-C chemokine receptor type 2 (CCR2) signaling axis is critically involved in angiogenesis and cellular invasion; however, the therapeutic potential of its targeted blockade on alveolar echinococcosis (AE) remains largely unexplored. This study aimed to determine whether RS504393, a selective CCR2 antagonist, can inhibit the progression of AE by blocking the CCL2-CCR2 axis and modulating its downstream pathogenic mechanisms.
methodsIn this study, bioinformatics analysis of the GSE124362 dataset was combined with molecular docking simulations. Liver tissues from patients with AE and from Echinococcus multilocularis-infected mice were examined through histopathological and immunohistochemical staining methods. Pathological alterations and parasitic load were assessed by Western blot and quantitative real-time PCR (RT-PCR). An in vitro co-culture model involving Echinococcus multilocularis protoscolex-stimulated endothelial progenitor cells (EPCs), JS1 hepatic stellate cells (JS1) and RAW264.7 macrophages was established to evaluate angiogenesis, fibrogenic activity and macrophage polarization.
resultsIntegrated bioinformatics and molecular docking analyses revealed CCL2-CCR2 overexpression and high-affinity binding during AE progression. Treatment with RS504393 significantly attenuated hepatic fibrosis, suppressed phosphoinositide 3-kinase (PI3K)-protein kinase B (AKT) pathway activation and reduced M2 macrophage polarization in central lesion tissue of E. multilocularis-infected mice . In vitro, RS504393 inhibited angiogenesis driven by EPCs, induced apoptosis in JS1 cells, and redirected macrophage polarization from the M2 towards a more anti-parasitic phenotype.
conclusionsCCR2 blockade with RS504393 attenuates AE progression by inhibiting PI3K-AKT signaling, suppressing angiogenesis and inducing stellate cell apoptosis, collectively reducing hepatic fibrosis and parasitic burden. Our findings provide a mechanistic rationale for repurposing CCR2 antagonists as a novel host-directed therapeutic strategy for echinococcosis.
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