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Updated: Aug 20, 2025
Phenotypic Characterization of Macrophages from Rat Kidney by Flow Cytometry
Published on: October 18, 2016
Treating crescentic glomerulonephritis by targeting macrophages
Anqun Chen1, Kyung Lee2, John Cijiang He3
1Department of Nephrology, Hunan Key Laboratory of Kidney Disease and Blood Purification, Institute of Nephrology, The Second Xiangya Hospital at Central South University, Changsha, Hunan, China.
Abstract:
Macrophage accumulation in the kidney is associated with the progression of crescentic glomerulonephritis (GN) and is mostly derived from circulating monocytes. FROUNT, a C-C motif chemokine receptor 2 (CCR2)-interacted protein, which is strongly expressed in monocytes/macrophages, enhances macrophage infiltration through CCR2-mediated chemotaxis. In this issue of the journal, Toda et al. reported that disulfiram, an inhibitor of FROUNT, attenuates GN by inhibition of the FROUNT-CCR2 interaction and macrophage migration and activation, suggesting a potential therapeutic role for crescentic GN.
Insights
Disulfiram, a FROUNT inhibitor, shows promise in treating crescentic glomerulonephritis (GN). It reduces kidney macrophage infiltration by blocking the FROUNT-CCR2 interaction, thereby inhibiting monocyte migration and activation.
Area of Science:
- Nephrology
- Immunology
- Pharmacology
Background:
- Macrophage accumulation in the kidney drives crescentic glomerulonephritis (GN) progression.
- Monocytes are the primary source of these infiltrating kidney macrophages.
- FROUNT protein enhances macrophage infiltration via the C-C motif chemokine receptor 2 (CCR2) pathway.
Purpose of the Study:
- To investigate the therapeutic potential of disulfiram, a FROUNT inhibitor, in treating crescentic GN.
- To elucidate the mechanism by which disulfiram affects macrophage infiltration and activation in GN.
Main Methods:
- Administration of disulfiram to inhibit FROUNT.
- Assessment of macrophage infiltration and activation in a crescentic GN model.
- Evaluation of the interaction between FROUNT and CCR2.
Main Results:
- Disulfiram treatment attenuated GN.
- Inhibition of the FROUNT-CCR2 interaction was observed.
- Disulfiram reduced macrophage migration and activation in the kidneys.
Conclusions:
- Disulfiram demonstrates a therapeutic effect in crescentic GN by inhibiting FROUNT.
- Targeting the FROUNT-CCR2 interaction offers a potential therapeutic strategy for GN.
- Disulfiram warrants further investigation as a treatment for crescentic GN.
