Linked Life Data

21249349

Source:http://linkedlifedata.com/resource/pubmed/id/21249349

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2011-3-9
pubmed:abstractText
The heart is a highly plastic organ. In response to the physiological stress of normal life, as well as the pathological stress of disease, the myocardium manifests robust and rapid changes in mass. In the context of disease-associated stress, this myocardial remodeling response can culminate in ventricular thinning, mechanical dysfunction, and a clinical syndrome of heart failure. Recently, autophagy, a process of cellular cannibalization, has been implicated in many of these remodeling reactions. In some settings, the autophagic response is beneficial and pro-survival; in other contexts, it is maladaptive and promotes disease progression. Together, these observations raise the intriguing prospect of targeting maladaptive autophagy and advancing cell survival-promoting, adaptive autophagy to benefit patients with heart disease.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
1432-1971
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
32
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
282-9
pubmed:meshHeading
pubmed:year
2011
pubmed:articleTitle
Autophagy in cardiac plasticity and disease.
pubmed:affiliation
Division of Cardiology, Department of Internal Medicine, University of Texas Southwestern Medical Center, NB11.200, 6000 Harry Hines Blvd, Dallas, TX 75390-8573, USA. joseph.hill@utsouthwestern.edu
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural