Oxidative stress and renal biology: Unraveling the bidirectional link with aging and chronic kidney disease
Excessive levels of reactive oxygen and nitrogen species cause cellular injury, termed oxidative stress. This occurs due to an imbalance between the prooxidant and antioxidant capabilities of the cell. Mounting evidence suggests a strong connection between aging, oxidative stress, and age-mediated diseases, including chronic kidney disease (CKD). The global prevalence of CKD has shown an increasing trend, especially among the elderly. Under physiological conditions, homeostatic mechanisms limit oxidative stress and repair oxidant-induced damage. However, in CKD, oxidative stress is not mitigated but worsened due to the disruption of homeostasis, particularly with aging. CKD also accelerates aging through several mechanisms, including oxidative stress. In turn, oxidative stress can contribute to CKD as the principal cellular factor. Besides, CKD and its comorbid conditions can result in inflammation, oxidative stress, apoptosis, and necrosis, which stimulate premature senescence in multiple body organs. Unraveling the potential mechanisms of CKD and the role of oxidative stress in CKD pathology in aging patients necessitates an inclusive discussion of current research. In this review, we summarize previous studies and discuss the role of oxidative stress and its implications in the pathogenesis of CKD during both premature and normal aging.
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