Kidney apoptosis and fibrosis are an inevitable outcome of progressive chronic kidney diseases where
congenital obstructive nephropathy is the primary cause of the end-stage renal disease in children, and is also a major
cause of renal failure in adults. The injured tubular cells linked to interstitial macrophages, and myofibroblasts produce
cytokines and growth factors that promote an inflammatory state in the kidney, induce tubular cell apoptosis, and facilitate
the accumulation of extracellular matrix. Angiotensin II plays a central role in the renal fibrogenesis at a very early stage
leading to a rapid progression in chronic kidney disease. The increasing levels of angiotensin II induce pro-inflammatory
cytokines, NF-κB activation, adhesion molecules, chemokines, growth factors, and oxidative stress. Furthermore, growing
evidence reports that angiotensin II (a pro-inflammatory hormone) increases the mitochondrial oxidative stress regulating
apoptosis induction. This review summarizes our understanding about possible mechanisms that contribute to apoptosis
modulated by inflammation and/or oxidative stress during obstructive nephropathy. The new concept of antiinflammatory
tools 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.
Keywords: Angiotensin II, apoptosis, mitochondria, obstructive nephropathy, oxidative stress, fibrosis, interstitial macrophages, tubular cells, cytokines, NF-kB activation
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