Oxidative Stress Mechanisms in Kidney Injury
Summary
The kidney relies on redox homeostasis to support filtration, reabsorption and excretion under high metabolic demand. Oxidative stress occurs when reactive oxygen species (ROS) generated by mitochondrial respiration, NADPH oxidases and endoplasmic reticulum stress exceed the capacity of endogenous defences such as superoxide dismutase, catalase and glutathione, causing lipid peroxidation, protein and DNA oxidation. These molecular insults provoke tubular epithelial injury, endothelial dysfunction and interstitial inflammation that drive apoptosis and fibrotic remodelling. Cellular pathways including nuclear factor erythroid 2-related factor 2 (Nrf2) and nuclear factor κB (NF-κB) orchestrate antioxidant responses and inflammatory signalling, respectively. Sustained imbalance predisposes to acute kidney injury and accelerates chronic kidney disease, posing a global health burden. Advances in redox biology have yielded novel biomarkers of oxidative damage, engineered nanoparticles and natural antioxidants designed to restore redox equilibrium and preserve renal integrity.
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Oxidative Stress Mechanisms in Kidney Injury publication trend
The graph below shows the total number of articles in oxidative stress mechanisms in kidney injury across all publications each year (not limited to Nature Index journals).
Technical terms
Reactive oxygen species (ROS): chemically reactive molecules containing oxygen that can oxidise cellular components.
Oxidative stress: imbalance between ROS generation and antioxidant defences leading to molecular damage.
Mitochondrial dysfunction: impairment of mitochondrial energy production that increases ROS output.
Nuclear factor erythroid 2-related factor 2 (Nrf2): transcription factor that activates genes encoding antioxidant enzymes.
Nanozyme: nanomaterial engineered to mimic enzyme-like antioxidant catalytic behaviour.
Klotho protein: anti-aging transmembrane protein that regulates antioxidant pathways and mitochondrial homeostasis.
References
- pH‐Activatable Pre‐Nanozyme Mediated H2S Delivery for Endo‐Exogenous Regulation of Oxidative Stress in Acute Kidney Injury. Advanced Science (2024).
- Klotho, Oxidative Stress, and Mitochondrial Damage in Kidney Disease. Antioxidants (2023).
- Molecular Mechanisms of Oxidative Stress in Acute Kidney Injury: Targeting the Loci by Resveratrol. International Journal of Molecular Sciences (2023).
- Oxidative Stress in the Pathophysiology of Kidney Disease: Implications for Noninvasive Monitoring and Identification of Biomarkers. Oxidative Medicine and Cellular Longevity (2020).
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