Linked Life Data

21482032

Source:http://linkedlifedata.com/resource/pubmed/id/21482032

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2011-6-7
pubmed:abstractText
Autophagy is a conserved catabolic process for long-lived proteins and organelles and is primarily responsible for nonspecific degradation of redundant or faulty cell components. Although autophagy has been described as the cell's major adaptive strategy in response to metabolic challenges, its influence on the cell's energy profile is poorly understood. In the myocardium, autophagy is active at basal levels and is crucial for maintaining its contractile function. Defects in the autophagic machinery cause cardiac dysfunction and heart failure. In this paper we propose that (1) autophagy contributes significantly to the metabolic balance sheet of the heart. (2) Increased autophagy contributes to an improved myocardial energy profile through changing the cardiac substrate preference. (3) Substrates generated through autophagy give rise to an alternative for ATP production with an oxygen-sparing effect. These elements identify autophagy in a new context of myocardial metabolic interregulation, which we discuss in the settings of myocardial infarction, heart failure and the diabetic heart. It is hoped that the hypothesis presented can lead to new insights aimed at exploiting autophagy to improve existing metabolic-based therapy in heart disease.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
1532-2777
pubmed:author
pubmed:copyrightInfo
Copyright © 2011 Elsevier Ltd. All rights reserved.
pubmed:issnType
Electronic
pubmed:volume
77
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
52-7
pubmed:meshHeading
pubmed:year
2011
pubmed:articleTitle
Autophagy in heart disease: a strong hypothesis for an untouched metabolic reserve.
pubmed:affiliation
Department of Physiological Sciences, Faculty of Natural Sciences, University of Stellenbosch, Stellenbosch 7600, South Africa. bloos@sun.ac.za
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't