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Autophagy in heart disease: A strong hypothesis for an untouched metabolic reserve

dc.contributor.authorLoos B.
dc.contributor.authorLochner A.
dc.contributor.authorEngelbrecht A.-M.
dc.date.accessioned2011-10-13T16:58:23Z
dc.date.available2011-10-13T16:58:23Z
dc.date.issued2011
dc.identifier.citationMedical Hypotheses
dc.identifier.citation77
dc.identifier.citation1
dc.identifier.citationhttp://www.scopus.com/inward/record.url?eid=2-s2.0-79958025505&partnerID=40&md5=a420e7d927d8a2f10a61c52e2e91d6c3
dc.identifier.issn3069877
dc.identifier.other10.1016/j.mehy.2011.03.021
dc.identifier.urihttp://hdl.handle.net/10019.1/16704
dc.description.abstractAutophagy 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. © 2011 Elsevier Ltd.
dc.subjectadenosine triphosphate
dc.subjectoxygen
dc.subjectarticle
dc.subjectautophagy
dc.subjectcell survival
dc.subjectdiabetic cardiomyopathy
dc.subjectenergy metabolism
dc.subjectheart disease
dc.subjectheart failure
dc.subjectheart infarction
dc.subjectheart muscle
dc.subjectheart muscle ischemia
dc.subjecthuman
dc.subjectmetabolic balance
dc.subjectnonhuman
dc.subjectprotein degradation
dc.titleAutophagy in heart disease: A strong hypothesis for an untouched metabolic reserve
dc.typeArticle
dc.description.versionArticle


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