Abstract:

Chronic Kidney Disease (CKD) affects millions of people worldwide and is a global health problem with few treatment options. The mechanisms underlying the pathogenesis of CKD include oxidative damage and inflammation. Damage to the glomeruli may be observed during the course of co-associated diseases such diabetes, but also in specific conditions such as focal segmental glomerulosclerosis. During its early manifestation, podocyte’s damage and death are key factors to glomerulopathies and its protection may represent an important therapeutic approach. Importantly, podocytes pathology involves inflammation and cellular damage, principally due to excessive oxidative stress. Underlying mechanisms associated to both inflammation and oxidative stress during the course of a renal lesion must be elucidated for the development of better clinical and research approaches to kidney physiology. Thus, here we discuss the role of the Thioredoxin system, an antioxidant mechanism, and TXNIP, a thioredoxin inhibitor linked to NRLP3 inflammasome activation, as a pivotal axis in the pathophysiology of glomerular lesions.

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