The circadian rhythm has a strong influence on both cardiac physiology and disease in humans. Preclinical studies primarily using tissue-specific transgenic mouse models have contributed to our understanding of the molecular mechanism of the circadian clock in the cardiovascular system. The core clock driven by CLOCK:BMAL1 complex functions as a universal timing machinery that primarily sets the pace in all mammalian cell types. In one specific cell or tissue type, core clock may control a secondary transcriptional oscillator, conceptualized as slave clock, which confers the oscillatory expression of tissue-specific effectors. Here, we discuss a core clock-slave clock-effectors network, which links the molecular clock to cardiac function.
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