Journal
FRONTIERS IN IMMUNOLOGY
Volume 13, Issue -, Pages -Publisher
FRONTIERS MEDIA SA
DOI: 10.3389/fimmu.2022.1015142
Keywords
diabetic nephropathy; macrophage; metabolic disorder; inflammation; fibrosis
Categories
Funding
- Shenzhen Science & Innovation Fund [JCYJ20180306173745092, JCYJ20210324114604013]
- HKSAR General Research Fund [17109019, 17113416]
- Seed Fund for Basic Research [202011159210, 202111159235]
- Research Start-up Foundation of Shenzhen University (SZU)
- Natural Science Foundation of Shenzhen University General Hospital [SUGH2020QD011, SUGH2020QD021]
- Science Technology and Innovation Committee of Shenzhen Municipality [JCYJ20210324094804013]
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Diabetic nephropathy is the most common chronic kidney disease, and the activation and transition of resident macrophages play a crucial role in causing renal inflammation and fibrosis. Inhibiting macrophage activation and macrophage-cell interactions may be a promising approach to attenuate diabetic nephropathy.
Diabetic nephropathy (DN) is the most common chronic kidney disease. Accumulation of glucose and metabolites activates resident macrophages in kidneys. Resident macrophages play diverse roles on diabetic kidney injuries by releasing cytokines/chemokines, recruiting peripheral monocytes/macrophages, enhancing renal cell injuries (podocytes, mesangial cells, endothelial cells and tubular epithelial cells), and macrophage-myofibroblast transition. The differentiation and cross-talks of macrophages ultimately result renal inflammation and fibrosis in DN. Emerging evidence shows that targeting macrophages by suppressing macrophage activation/transition, and macrophages-cell interactions may be a promising approach to attenuate DN. In the review, we summarized the diverse roles of macrophages and the cross-talks to other cells in DN, and highlighted the therapeutic potentials by targeting macrophages.
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