Macrophage-Mediated Inflammation in Diabetic Kidney Disease
Summary
Diabetic kidney disease (DKD) is a major microvascular complication of diabetes mellitus, characterised by progressive glomerulosclerosis, tubulointerstitial inflammation and eventual loss of renal function. Chronic hyperglycaemia and associated metabolic stress promote oxidative injury and haemodynamic alterations that trigger the recruitment and activation of innate immune cells. Among these, macrophages assume central roles through dynamic polarisation into pro-inflammatory (M1) and reparative (M2) phenotypes. M1 macrophages secrete cytokines and chemokines that exacerbate podocyte and endothelial injury, while M2 macrophages contribute to wound healing but, when dysregulated, drive excessive extracellular matrix deposition and fibrosis. The balance between these opposing states determines whether inflammation resolves or progresses to irreversible scarring. Recent advances in imaging, molecular profiling and functional studies have illuminated the heterogeneity of renal macrophages, revealing new mechanistic insights and opening avenues for therapies that target macrophage-mediated pathways to slow or halt DKD progression.
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Macrophage-Mediated Inflammation in Diabetic Kidney Disease publication trend
The graph below shows the total number of articles in macrophage-mediated inflammation in diabetic kidney disease across all publications each year (not limited to Nature Index journals).
Technical terms
Macrophage: A versatile innate immune cell responsible for phagocytosis, antigen presentation and secretion of mediators that orchestrate inflammation and repair.
Polarization: The process by which macrophages adopt distinct activation states—classically activated (M1) or alternatively activated (M2)—with divergent inflammatory or reparative roles.
Cytokine: A small protein released by immune and other cells to regulate inflammation, cell recruitment and tissue responses.
Fibrosis: Excessive deposition of extracellular matrix proteins resulting in organ scarring and functional decline.
Hyperglycaemia: Elevated blood glucose levels that drive metabolic disturbances and tissue damage in diabetes.
References
- Unraveling the Role of Inflammation in the Pathogenesis of Diabetic Kidney Disease. International Journal of Molecular Sciences (2019).
- Macrophage Phenotype and Fibrosis in Diabetic Nephropathy. International Journal of Molecular Sciences (2020).
- Single-cell RNA and transcriptome sequencing profiles identify immune-associated key genes in the development of diabetic kidney disease. Frontiers in Immunology (2023).
- Excessive Activation of Notch Signaling in Macrophages Promote Kidney Inflammation, Fibrosis, and Necroptosis. Frontiers in Immunology (2022).
- Targeting Macrophages: Therapeutic Approaches in Diabetic Kidney Disease. International Journal of Molecular Sciences (2024).
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