Good and bad consequences of altered fatty acid metabolism in heart failure: evidence from mouse models

被引：89

作者：

Abdurrachim, Desiree ^{[1
]}

Luiken, Joost J. F. P. ^{[2
]}

Nicolay, Klaas ^{[1
]}

Glatz, Jan F. C. ^{[2
]}

Prompers, Jeanine J. ^{[1
]}

Nabben, Miranda ^{[1
,2
]}

机构：

[1] Eindhoven Univ Technol, Dept Biomed Engn, Biomed NMR, NL-5600 MB Eindhoven, Netherlands

[2] Maastricht Univ, Dept Genet & Cell Biol, Cardiovasc Res Inst Maastricht CARIM, NL-6200 MD Maastricht, Netherlands

来源：

CARDIOVASCULAR RESEARCH | 2015年 / 106卷 / 02期

关键词：

Heart failure; Energy metabolism; Genetically altered mice; Metabolic shift; ACTIVATED-RECEPTOR-ALPHA; TRANSCRIPTIONAL COACTIVATOR PGC-1-ALPHA; LIPASE OVEREXPRESSION PROTECTS; MITOCHONDRIAL BETA-OXIDATION; CARDIAC GLUCOSE-OXIDATION; ACETYL-COA CARBOXYLASE; PRESSURE-OVERLOAD; CONTRACTILE FUNCTION; KNOCKOUT MICE; DILATED CARDIOMYOPATHY;

D O I：

10.1093/cvr/cvv105

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

The shift in substrate preference away from fatty acid oxidation (FAO) towards increased glucose utilization in heart failure has long been interpreted as an oxygen-sparing mechanism. Inhibition of FAO has therefore evolved as an accepted approach to treat heart failure. However, recent data indicate that increased reliance on glucose might be detrimental rather than beneficial for the failing heart. This review discusses new insights into metabolic adaptations in heart failure. A particular focus lies on data obtained from mouse models with modulations of cardiac FA metabolism at different levels of the FA metabolic pathway and how these differently affect cardiac function. Based on studies in which these mouse models were exposed to ischaemic and non-ischaemic heart failure, we discuss whether and when modulations in FA metabolism are protective against heart failure.

引用

页码：194 / 205

页数：12

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