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Review
. 2010 Mar 5;106(4):647-58.
doi: 10.1161/CIRCRESAHA.109.209957.

The cardiomyocyte circadian clock: emerging roles in health and disease

David J Durgan  1 , Martin E Young
Affiliations
Review

The cardiomyocyte circadian clock: emerging roles in health and disease

David J Durgan et al. Circ Res. .

Abstract

Circadian misalignment has been implicated in the development of obesity, diabetes mellitus, and cardiovascular disease. Time-of-day-dependent synchronization of organisms with their environment is mediated by circadian clocks. This cell autonomous mechanism has been identified within all cardiovascular-relevant cell types, including cardiomyocytes. Recent molecular- and genetic-based studies suggest that the cardiomyocyte circadian clock influences multiple myocardial processes, including transcription, signaling, growth, metabolism, and contractile function. Following an appreciation of its physiological roles, the cardiomyocyte circadian clock has recently been linked to the pathogenesis of heart disease in response to adverse stresses, such as ischemia/reperfusion, in animal models. The purpose of this review is therefore to highlight recent advances regarding the roles of the cardiomyocyte circadian clock in both myocardial physiology and pathophysiology (ie, health and disease).

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Figures

Figure 1
Figure 1
Integration of Metabolism within the Mammalian Circadian Clock. Figure summarizes a large number of distinct studies highlighting metabolic loops within the mammalian circadian clock (see section entitled Heart Metabolism). Solid lines represent direct effects/links; dashed lines represent multiple steps; dotted lines (with ‘?’) represent hypothetical links. Ac represents acetyl group on an acetylated protein; ProX represents an undefined protein. Other definitions are included in the List of Abbreviations.
Figure 2
Figure 2
Hypothetical Model for the Regulation of Myocardial I/R Tolerance by the Cardiomyocyte Circadian Clock. GSK-3β, in its dephosphorylated and active form, promotes mPTP opening in response to stresses such as ischemia/reperfusion, and subsequent cell death. Inhibition of GSK-3β, through Akt-mediated phosphorylation, for example, limits mPTP opening. Akt may also promote cardioprotection through GSK-3β independent mechanisms. The cardiomyocyte circadian clock modulates Akt and GSK3β activity, which potentially mediates time-of-day-dependent oscillations in myocardial ischemia/reperfusion tolerance.
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