Oxidative Stress and Inflammation in Diabetic Nephropathy
Summary
Diabetic nephropathy arises from persistent hyperglycaemia, which drives excessive production of reactive oxygen species and the accumulation of advanced glycation end products. These disturbances disrupt redox homeostasis, activate pro-inflammatory pathways and impair antioxidant defences in glomerular and tubular cells. The ensuing oxidative stress and cytokine release provoke endothelial dysfunction, mesangial expansion and tubular atrophy, fostering extracellular matrix deposition and fibrosis. Understanding the interplay between oxidative damage and inflammation is essential for identifying biomarkers of early renal injury and for developing targeted interventions to slow or reverse disease progression.
Research from Nature Portfolio
Recent studies have revealed that coagulation factor XII is ectopically expressed by renal tubular cells in diabetic kidney disease and correlates with functional decline. In rodent models, genetic deletion of F12 or pharmacological blockade of its interaction with urokinase-type plasminogen activator receptor (uPAR) attenuates integrin β1-mediated signalling, reducing oxidative stress, DNA damage and cellular senescence in tubules. These findings implicate an unexpected FXII–uPAR–integrin axis in the pathogenesis of diabetic nephropathy and suggest novel diagnostic markers and therapeutic targets.
Oxidative Stress and Inflammation in Diabetic Nephropathy publication trend
The graph below shows the total number of articles in oxidative stress and inflammation in diabetic nephropathy across all publications each year (not limited to Nature Index journals).
Technical terms
Reactive Oxygen Species (ROS): Highly reactive oxygen-derived molecules that can damage lipids, proteins and DNA when antioxidant defences are overwhelmed.
Advanced Glycation End Products (AGEs): Irreversible adducts formed by non-enzymatic glycation of proteins or lipids, which promote oxidative stress and inflammation.
Urokinase-type Plasminogen Activator Receptor (uPAR): A cell-surface receptor that coordinates protease activity and integrin signalling, influencing inflammation and fibrosis.
Endoplasmic Reticulum (ER) Stress: A cellular condition triggered by accumulation of unfolded proteins in the ER, which activates adaptive or apoptotic pathways.
References
- Factor XII signaling via uPAR-integrin β1 axis promotes tubular senescence in diabetic kidney disease. Nature Communications (2024).
- The UDPase ENTPD5 regulates ER stress-associated renal injury by mediating protein N-glycosylation. Cell Death & Disease (2023).
- Oxidative Stress in Diabetic Nephropathy with Early Chronic Kidney Disease. Journal of Diabetes Research (2016).
- Inflammatory Cytokines in Diabetic Nephropathy. Journal of Diabetes Research (2015).
- Inflammation and Oxidative Stress in Diabetic Nephropathy: New Insights on Its Inhibition as New Therapeutic Targets. Journal of Diabetes Research (2013).
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