Apoptosis Modulated by Oxidative Stress and Inflammation During Obstructive Nephropathy

MANUCHA WALTER; GARRAMUÑO VALLÉS , PATRICIA

Inflammation & allergy - drug targets

Bentham Science Publishers

Lugar: San Francisco, CA ; Año: 2012 vol. 11 p. 303 - 312

1871-5281

Abstract: Kidney apoptosis and fibrosis are an inevitable outcome of progressive chronic kidney diseases wherecongenital obstructive nephropathy is the primary cause of the end-stage renal disease in children, and is also a majorcause of renal failure in adults. The injured tubular cells linked to interstitial macrophages, and myofibroblasts producecytokines and growth factors that promote an inflammatory state in the kidney, induce tubular cell apoptosis, and facilitatethe accumulation of extracellular matrix. Angiotensin II plays a central role in the renal fibrogenesis at a very early stageleading to a rapid progression in chronic kidney disease. The increasing levels of angiotensin II induce pro-inflammatorycytokines, NF-􀀃B activation, adhesion molecules, chemokines, growth factors, and oxidative stress. Furthermore, growingevidence reports that angiotensin II (a pro-inflammatory hormone) increases the mitochondrial oxidative stress regulatingapoptosis induction. This review summarizes our understanding about possible mechanisms that contribute to apoptosismodulated by inflammation and/or oxidative stress during obstructive nephropathy. The new concept of antiinflammatorytools regulating mitochondrial oxidative stress will directly affect the inflammatory process and apoptosis.This idea could have attractive consequences in the treatment of renal and other inflammatory pathologies.