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Trends Endocrinol Metab. 2015 Jan;26(1):40-8. doi: 10.1016/j.tem.2014.11.001. Epub 2014 Nov 28.

Is AMPK the savior of the failing heart?

Author information

1
Cardiovascular Research Centre, Mazankowski Alberta Heart Institute, Department of Pediatrics, Faculty of Medicine and Dentistry, 458 Heritage Medical Research Centre, University of Alberta, Edmonton, AB, T6G 2S2, Canada.
2
Cardiovascular Research Centre, Mazankowski Alberta Heart Institute, Department of Pediatrics, Faculty of Medicine and Dentistry, 458 Heritage Medical Research Centre, University of Alberta, Edmonton, AB, T6G 2S2, Canada. Electronic address: jason.dyck@ualberta.ca.

Abstract

Heart failure (HF) is one of the leading causes of death, affecting more than 20 million people worldwide. A vast array of pathophysiological and molecular events contributes to the development and eventual worsening of HF. Of these, defects in myocardial metabolic processes that normally result in proper ATP production necessary to maintain contractile function appear to be a major contributor to HF pathogenesis. A key player involved in regulating myocardial metabolism is AMP-activated protein kinase (AMPK), a major regulatory kinase controlling numerous metabolic pathways. Here, we review the metabolic changes that occur in HF, what role alterations in energy metabolism has in its progression, and the involvement of AMPK in this context.

KEYWORDS:

AMP-activated protein kinase (AMPK); cardiac metabolism; myocardial ATP production; systolic heart failure

PMID:
25439672
DOI:
10.1016/j.tem.2014.11.001
[Indexed for MEDLINE]

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