Nitric oxide and oxidative stress in cardiovascular aging.
The long-standing free radical theory of aging, which attributes cellular pathology to the relentless accumulation of reactive oxygen species (ROS), remains attractive but controversial. Emerging insights into the molecular interactions between ROS and reactive nitrogen species (RNS) such as nitric oxide suggest that, in biological systems, one effect of increased ROS is the disruption of protein S-nitrosylation, a ubiquitous posttranslational modification system. In this way, ROS may not only damage cells but also disrupt widespread signaling pathways. Here, we discuss this phenomenon in the context of the cardiovascular system and propose that ideas regarding oxidative stress and aging need to be reevaluated to take account of the balance between oxidative and nitrosative stress.
Raju
Shubha V Y
SV
Cardiology Division, Department of Medicine, The Johns Hopkins Hospital, 720 Rutland Avenue, Baltimore, MD 21205, USA.
Barouch
Lili A
LA
Hare
Joshua M
JM
D000375:Aging / Q000502:physiology*; D017209:Apoptosis; D002318:Cardiovascular Diseases / Q000503:physiopathology; D006801:Humans; D008136:Longevity / Q000235:genetics; D008928:Mitochondria / Q000502:physiology; D009569:Nitric Oxide; D018384:Oxidative Stress; D011499:Protein Processing, Post-Translational; D017382:Reactive Oxygen Species / Q000009:adverse effects*
D017382:Reactive Oxygen Species; D009569:Nitric Oxide