LAUSR

Cardiovascular disease (CVD) are complex multi-factorial disorders that constitutes the leading cause of morbidity and mortality worldwide (Roth et al., 2020). Homeostatic heart function depends on several key physiological parameters such as cardiac contractility, metabolic state and overall effective hemodynamic regulation of the body (Verbrugge et al., 2020). Mammalian circadian (~24 h) clocks are ubiquitous autoregulatory molecular interactive transcriptional/translational feedback loops that precisely drive diverse daily physiological processes. Centrally, the suprachiasmatic nucleus (SCN) in the brain respond to light entrainment, and act as a pacemaker of the circadian timing in the body. At a molecular level, each cell possesses clock genes which are regulated by a variety of SCN-derived periodical stimulants and act as peripheral clocks. Heterodimers of central clock factors (CLOCK and BMAL1) bind to E-boxes within diverse target gene promoters including the clock genes Per and Cry. PER and CRY then dimerize and repress their own transcription by inhibiting CLOCK:BMAL1. CLOCK:BMAL1 also induce the expression of REV-ERBα, which represses Bmal1 transcription (Takahashi, 2017). The precise orchestration of this interlocking feedback loop regulates many fundamental aspects of cardiovascular processes such as daily rhythms in blood pressure and heart rate, electrophysiology, cardiac metabolism and contractility, endothelial cell biology, platelet aggregation, and thrombus formation are also influenced by the local intrinsic circadian clock. Circadian misalignment or clock dysfunction can lead to diverse cardiovascular diseases such as cardiac arrhythmias, cardiomyopathy and diabetes (Martino and Young, 2015; Alibhai et al., 2017; Thosar et al., 2018; Chellappa et al., 2019; Crnko et al., 2019; Rana et al., 2020). The occurrence of adverse cardiovascular events such as acute heart failure, myocardial infarction, stroke, and cardiac arrhythmias, also exhibits a daily variation with prevalence in the early morning hours (Cohen et al., 1997). The purpose of this Research Topic is to highlight the impact of the circadian axis on the regulation of cardiac function and disease, including its interaction with feeding behaviour, electrophysiology, pathogenesis of cardiac disease and mechanisms of cardio-protection and repair. Schroder and Delisle reviewed the impact of feeding behaviour on circadian cardiac physiology. Restricted feeding studies have been used to disentangle the interconnections between the cellular circadian clocks, physiological circadian rhythms (such as change in heart OPEN ACCESS