EMERGING ROLE OF MITOCHONDRIA AND OXIDATIVE STRESS IN RENAL INFLAMMATORY PROCESSES

WALTER MANUCHA

Chascomús, Buenos Aires

Jornada; XVI Jornadas Anuales de la Sociedad Argentina de Biología; 2014

Sociedad Argentina de Biología

Chronic kidney disease involves both programmed cell death and fibrosis. Both phenomena may be closely related to the recently described dysregulation, associated with oxidative stress, of the mitochondrial machinery in patients with chronic kidney disease. Injured tubule cells, attached to interstitial macrophages and myofibroblasts, release cytokines and growth factors that promote an inflammatory state, induce tubular cell apoptosis and lead to the accumulation of extracellular matrix. Angiotensin II plays a central role in renal fibrogenesis, leading to a fast and unrelenting progression of chronic kidney disease. High angiotensin II levels lead to increased expression of NF-KB, adhesion molecules, chemokines and growth factors, with release of inflammatory cytokines and oxidative stress. All current evidence suggests that angiotensin II increases mitochondrial oxidative stress, leads to the induction of apoptosis and allows the build-up and perpetuation of a chronic inflammatory state. Since mitochondrial dysfunction and oxidative stress have a major role in the pathogenesis of renal inflammatory processes, a set of anti-inflammatory tools against the mitochondrial oxidative stress causing apoptosis and perpetuating inflammation may be advanced as a novel therapeutic approach. This may open new perspectives of treatment for inflammatory kidney disease and related conditions.