Oxidative stress has been implicated in the pathophysiology of diabetic nephropathy. Studies in experimental animal models of diabetes strongly implicate oxidant species as a major determinant in the pathophysiology of diabetic kidney disease. The translation, in the clinical setting, of these concepts have been quite disappointing, and new theories have challenged the concepts that oxidative stress per se plays a role in the pathophysiology of diabetic kidney disease. The concept of mitochondrial hormesis has been introduced to explain this apparent disconnect. Hormesis is intended as any cellular process that exhibits a biphasic response to exposure to increasing amounts of a substance or condition: specifically, in diabetic kidney disease, oxidant species may represent, at determined concentration, an essential and potentially protective factor. It could be postulated that excessive production or inhibition of oxidant species formation might result in an adverse phenotype. This review discusses the evidence underlying these two apparent contradicting concepts, with the aim to propose and speculate on potential mechanisms underlying the role of oxidant species in the pathophysiology of diabetic nephropathy and possibly open future more efficient therapies to be tested in the clinical settings.
Keywords: Diabetes; Kidney; Oxidative stress.
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