Treating crescentic glomerulonephritis by targeting macrophages

Anqun Chen; Kyung Lee; John Cijiang He

doi:10.1016/j.kint.2022.09.004

Treating crescentic glomerulonephritis by targeting macrophages

Kidney Int. 2022 Dec;102(6):1212-1214. doi: 10.1016/j.kint.2022.09.004.

Authors

Anqun Chen¹, Kyung Lee², John Cijiang He³

Affiliations

¹ Department 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. Electronic address: anqunchen@163.com.
² Division of Nephrology, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
³ Division of Nephrology, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York, USA; Renal Program, James J. Peters Veterans Affairs Medical Center at Bronx, Bronx, New York, USA. Electronic address: cijiang.he@mssm.edu.

PMID: 36411015
DOI: 10.1016/j.kint.2022.09.004

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.

Publication types

Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Research Support, N.I.H., Extramural
Comment

MeSH terms

Chemotaxis
Glomerulonephritis* / drug therapy
Glomerulonephritis* / metabolism
Humans
Macrophages / metabolism
Monocytes / metabolism
Receptors, CCR2* / metabolism

Substances

Receptors, CCR2

Abstract

Publication types

MeSH terms

Substances

Grants and funding