The PPAR trio: Regulators of myocardial energy metabolism in health and disease

Abstract Common causes of heart failure are associated with derangements in myocardial fuel utilization. Evidence is emerging that metabolic abnormalities may contribute to the development and progression of myocardial disease. The peroxisome proliferator-activated receptor (PPAR) family of nuclear...

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Bibliographic Details
Published in:Journal of molecular and cellular cardiology 2008-06, Vol.44 (6), p.968-975
Main Authors: Madrazo, Jose A, Kelly, Daniel P
Format: Article
Language:English
Subjects:
Animals
Cardiomyopathy
Cardiovascular
Diabetes
Diabetes Mellitus - genetics
Diabetes Mellitus - metabolism
Energy Metabolism - genetics
Fatty Acid
Fatty Acids - genetics
Fatty Acids - metabolism
Gene Expression Regulation - genetics
Glucose
Glucose - genetics
Glucose - metabolism
Heart Failure - genetics
Heart Failure - metabolism
Humans
Hypertension - genetics
Hypertension - metabolism
Metabolism
Mice
Murine model
Myocardium - metabolism
Peroxisome proliferator-activated receptor (PPAR)
Peroxisome Proliferator-Activated Receptors - genetics
Peroxisome Proliferator-Activated Receptors - metabolism
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Summary:Abstract Common causes of heart failure are associated with derangements in myocardial fuel utilization. Evidence is emerging that metabolic abnormalities may contribute to the development and progression of myocardial disease. The peroxisome proliferator-activated receptor (PPAR) family of nuclear receptor transcription factors has been shown to regulate cardiac fuel metabolism at the gene expression level. The three PPAR family members (alpha, beta/delta and gamma) are uniquely suited to serve as transducers of developmental, physiological, and dietary cues that influence cardiac fatty acid and glucose metabolism. This review describes murine PPAR loss- and gain-of-function models that have shed light on the roles of these receptors in regulating myocardial metabolic pathways and have defined key links to disease states including the hypertensive and diabetic heart.
ISSN:0022-2828
1095-8584
DOI:10.1016/j.yjmcc.2008.03.021