SCIENCE@home

Dectin-1 is Pathogenic in Chronic Kidney Disease by Promoting Macrophage Infiltration and Transition to Myofibroblast

Lingling Shen,Jingyi Li,Anqi Zhang,Sijing Yan,Wenxin Sha,Yucheng Wang,Shi Feng,Cuili Wang,Zhimin Chen,Hongfeng Huang,Bingjue Li,Ping-ping Ren,Suhan Zhou,Siqi Wu,Yanli Wang,Zhouji Shen,Song Rong,Hermann Haller,Hong Jiang,Jianghua Chen

Published 2025 in International Journal on Biological Sciences

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.

PUBLICATION RECORD

CITATION MAP

EXTRACTION MAP

CLAIMS

  • No claims are published for this paper.

CONCEPTS

  • No concepts are published for this paper.

REFERENCES

Showing 1-43 of 43 references · Page 1 of 1

CITED BY