The interaction between the renin angiotensin system and peroxisome proliferatior activated receptor: a hypothesis including mitochondria in aging.

ELENA MV DE CAVANAGH; BARBARA PIOTRKOWSKI; CESAR G FRAGA

Frontiers in Bioscience

Año: 2006 p. 1 - 18

The objective of improving health is intimately associated with preventing and delaying age-associated diseases. Nutritional and pharmacological approaches aimed at retarding aging are uncovering  pathways, whose  roles  in cell and tissue physiology need to be defined. In this article we hypothesize that peroxisome proliferator activated receptor (PPAR)-modulation is a pivotal process that underlies the association between mitochondria and the renin-angiotensin system (RAS) in aging. This hypothesis is based on several lines of evidence suggesting that: a) mitochondrial function and oxidant production are key players  in the aging process; b) PPARs, by regulating mitochondrial function and uncoupling proteins (UCP),  play a major role in the age-retarding effects of caloric restriction; c) RAS inhibition delays the deleterious effects of aging and also upregulates PPARs; and d) a number of physiological and molecular events that occur in experimental caloric restriction, and experimental and clinical RAS inhibition, involve changes in mitochondrial functions.