Linked Life Data

15917507

Source:http://linkedlifedata.com/resource/pubmed/id/15917507

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
21
pubmed:dateCreated
2005-5-26
pubmed:abstractText
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
1539-6150
pubmed:author
pubmed:issnType
Electronic
pubmed:day
25
pubmed:volume
2005
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
re4
pubmed:meshHeading
pubmed:year
2005
pubmed:articleTitle
Nitric oxide and oxidative stress in cardiovascular aging.
pubmed:affiliation
Cardiology Division, Department of Medicine, The Johns Hopkins Hospital, 720 Rutland Avenue, Baltimore, MD 21205, USA.
pubmed:publicationType
Journal Article, Review