ArticleInternational journal of biological sciences2025
Dectin-1 is Pathogenic in Chronic Kidney Disease by Promoting Macrophage Infiltration and Transition to Myofibroblast.
Article in International journal of biological sciences, 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.
- Spatiotemporal Control of Intercellular Crosstalk: A New Therapeutic Paradigm for Halting Acute Kidney Injury to Chronic Kidney Disease Transition.Biomolecules · 2026Review
- The Mechanism and Application of Traditional Chinese Medicine Nano-Formulations in the Treatment of Renal Fibrosis.International journal of nanomedicine · 2026Review
- Comment on "Dectin-1 is Pathogenic in Chronic Kidney Disease by Promoting Macrophage Infiltration and Transition to Myofibroblast".International journal of biological sciences · 2026Article
- RP-182 alleviated obstruction-induced renal fibrosis by reprogramming CD206Frontiers in pharmacology · 2026Article
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20 authors.
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Abstract
Dectin-1, a pattern recognition receptor predominantly expressed on myeloid cells, is required for maintaining immune homeostasis. However, the role of Dectin-1 in chronic kidney disease (CKD) remains unknown. Here we reported that Dectin-1 was markedly upregulated in the fibrotic kidneys of CKD patients, primarily in macrophages, and its expression correlated with fibrosis severity and renal dysfunction. Genetic deletion of Dectin-1 attenuated renal fibrosis induced by unilateral ureteral obstruction (UUO) or ischemia-reperfusion (IR), a finding confirmed in bone marrow chimeric mice. Macrophage-specific Dectin-1 deletion similarly protected against renal fibrosis, demonstrating its cell-autonomous role. Mechanistically, Dectin-1 promoted macrophage infiltration via Syk/NF-κB/CCL2-CCR2 axis, while facilitating macrophage-to-myofibroblast transition (MMT) by activating TGF-β/Smad signaling. Pre-clinically, pharmacological inhibition of Dectin-1 with Laminarin significantly reduced renal fibrosis in UUO and IR models, highlighting its therapeutic potential for CKD.
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