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Article: Targeting fatty acid and carbohydrate oxidation - A novel therapeutic intervention in the ischemic and failing heart

TitleTargeting fatty acid and carbohydrate oxidation - A novel therapeutic intervention in the ischemic and failing heart
Authors
Issue Date2011
Citation
Biochimica et Biophysica Acta - Molecular Cell Research, 2011, v. 1813 n. 7, p. 1333-1350 How to Cite?
AbstractCardiac ischemia and its consequences including heart failure, which itself has emerged as the leading cause of morbidity and mortality in developed countries are accompanied by complex alterations in myocardial energy substrate metabolism. In contrast to the normal heart, where fatty acid and glucose metabolism are tightly regulated, the dynamic relationship between fatty acid β-oxidation and glucose oxidation is perturbed in ischemic and ischemic-reperfused hearts, as well as in the failing heart. These metabolic alterations negatively impact both cardiac efficiency and function. Specifically there is an increased reliance on glycolysis during ischemia and fatty acid β-oxidation during reperfusion following ischemia as sources of adenosine triphosphate (ATP) production. Depending on the severity of heart failure, the contribution of overall myocardial oxidative metabolism (fatty acid β-oxidation and glucose oxidation) to adenosine triphosphate production can be depressed, while that of glycolysis can be increased. Nonetheless, the balance between fatty acid β-oxidation and glucose oxidation is amenable to pharmacological intervention at multiple levels of each metabolic pathway. This review will focus on the pathways of cardiac fatty acid and glucose metabolism, and the metabolic phenotypes of ischemic and ischemic/reperfused hearts, as well as the metabolic phenotype of the failing heart. Furthermore, as energy substrate metabolism has emerged as a novel therapeutic intervention in these cardiac pathologies, this review will describe the mechanistic bases and rationale for the use of pharmacological agents that modify energy substrate metabolism to improve cardiac function in the ischemic and failing heart. This article is part of a Special Issue entitled: Mitochondria and Cardioprotection. © 2011 Elsevier B.V.
Persistent Identifierhttp://hdl.handle.net/10722/195860
ISSN
2015 Impact Factor: 5.128
2015 SCImago Journal Rankings: 3.043
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorJaswal, JS-
dc.contributor.authorKeung, W-
dc.contributor.authorWang, W-
dc.contributor.authorUssher, JR-
dc.contributor.authorLopaschuk, GD-
dc.date.accessioned2014-03-19T01:46:11Z-
dc.date.available2014-03-19T01:46:11Z-
dc.date.issued2011-
dc.identifier.citationBiochimica et Biophysica Acta - Molecular Cell Research, 2011, v. 1813 n. 7, p. 1333-1350-
dc.identifier.issn0167-4889-
dc.identifier.urihttp://hdl.handle.net/10722/195860-
dc.description.abstractCardiac ischemia and its consequences including heart failure, which itself has emerged as the leading cause of morbidity and mortality in developed countries are accompanied by complex alterations in myocardial energy substrate metabolism. In contrast to the normal heart, where fatty acid and glucose metabolism are tightly regulated, the dynamic relationship between fatty acid β-oxidation and glucose oxidation is perturbed in ischemic and ischemic-reperfused hearts, as well as in the failing heart. These metabolic alterations negatively impact both cardiac efficiency and function. Specifically there is an increased reliance on glycolysis during ischemia and fatty acid β-oxidation during reperfusion following ischemia as sources of adenosine triphosphate (ATP) production. Depending on the severity of heart failure, the contribution of overall myocardial oxidative metabolism (fatty acid β-oxidation and glucose oxidation) to adenosine triphosphate production can be depressed, while that of glycolysis can be increased. Nonetheless, the balance between fatty acid β-oxidation and glucose oxidation is amenable to pharmacological intervention at multiple levels of each metabolic pathway. This review will focus on the pathways of cardiac fatty acid and glucose metabolism, and the metabolic phenotypes of ischemic and ischemic/reperfused hearts, as well as the metabolic phenotype of the failing heart. Furthermore, as energy substrate metabolism has emerged as a novel therapeutic intervention in these cardiac pathologies, this review will describe the mechanistic bases and rationale for the use of pharmacological agents that modify energy substrate metabolism to improve cardiac function in the ischemic and failing heart. This article is part of a Special Issue entitled: Mitochondria and Cardioprotection. © 2011 Elsevier B.V.-
dc.languageeng-
dc.relation.ispartofBiochimica et Biophysica Acta - Molecular Cell Research-
dc.titleTargeting fatty acid and carbohydrate oxidation - A novel therapeutic intervention in the ischemic and failing heart-
dc.typeArticle-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1016/j.bbamcr.2011.01.015-
dc.identifier.pmid21256164-
dc.identifier.scopuseid_2-s2.0-79957937929-
dc.identifier.hkuros239595-
dc.identifier.volume1813-
dc.identifier.issue7-
dc.identifier.spage1333-
dc.identifier.epage1350-
dc.identifier.isiWOS:000292177300011-

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