ArticleCellular and molecular life sciences : CMLS2025
CXCL12/CXCR4 modulates macrophage efferocytosis to induce glomerular crescent formation and fibrosis via ELMO1/DOCK180/RAC1 signaling in ANCA-associated glomerulonephritis.
Article in Cellular and molecular life sciences : CMLS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- ELMO1 and Rac1 Signaling in Kidney Disease: Molecular Mechanisms, Context-Dependent Roles, and Therapeutic Potential.Biomedicines · 2026Review
- Defective efferocytosis in diabetes: molecular mechanisms and emerging therapeutic strategies.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Efferocytosis: unifying pathogenic hub in metabolic disorders-mechanistic landscapes, targeted therapies and translational bottlenecks.Frontiers in immunology · 2026Review
- Integrated Transcriptomic and Machine Learning Analyses Identify KCNN3 and TLR10 as Candidate Cell-Type-Associated Molecules in Idiopathic Membranous Nephropathy.International journal of general medicine · 2026Article
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Authors and funding
13 authors.
Funding
Abstract
backgroundANCA-associated glomerulonephritis (AAGN) is a leading cause of uremia in children, driven by macrophages (Mφs) that mediate crescent formation and fibrosis. Despite their critical role, the signals governing monocyte recruitment and macrophage polarization in AAGN remain unclear.
methodsWe utilized single-cell sequencing to dissect the cellular dynamics of AAGN and conducted in vitro and in vivo experiments to explore the role of the CXCL12/CXCR4 signaling axis in monocyte recruitment and macrophage efferocytosis. Protein interaction analyses further delineated the downstream signaling pathways involved.
resultsCXCL12, released by apoptotic glomerular endothelial cells, recruited CXCR4
conclusionsThis study revealed that CXCL12/CXCR4 signaling axis plays a key regulatory role in the pathological process of AAGN. By establishing the specific molecular dialogue mechanism between endothelial cells and monocytes/macrophages, CXCL12 released by apoptotic endothelial cells can activate the CXCR4 on the surface of monocytes/macrophages, thereby promoting monocyte migration, enhancing macrophage-mediated efferocytosis and transforming into a pro-fibrotic phenotype. Targeted intervention with CXCL12/CXCR4 provides a promising approach for the treatment of AAGN.
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Registered trials
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