GPR183 contributes to renal macrophage infiltration and fibrosis in kidney injury

American Journal of Physiology-Renal Physiology 2026 Open access

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Authors: Qian Zhang, Yan Wang, Yu Fan, Seung Seok Han, Han Xie, Eugene P. Rhee, Donghai Wen
DOI: 10.1152/ajprenal.00037.2026
Cited by: 1
References: 45

Abstract

This study identifies GPR183 as a previously unrecognized regulator of macrophage polarization and renal fibrogenesis. We demonstrate that kidney injury activates an oxysterol-GPR183 signaling axis that promotes NF-κB-dependent M1 macrophage polarization. Genetic deletion of GPR183 selectively limits inflammatory macrophage accumulation, attenuates fibrosis, and preserves renal function, establishing GPR183 as a novel therapeutic target in progressive kidney disease.

Fields of Study & Subjects

Cholesterol and Lipid Metabolism Chronic Kidney Disease and Diabetes Immune cells in cancer

Publication details

Journal / source
American Journal of Physiology-Renal Physiology
Publisher
American Physiological Society
Volume
330
Issue
5
Pages
F619–F630
Publication date
9 April 2026
Language
EN