Circadian Dysregulation in Obesity: Unravelling Its Impact on Cardiovascular Risk and Therapeutic Strategies

Obesity is a global epidemic with significant implications for cardiovascular health, presenting a complex interplay of metabolic, inflammatory, and hemodynamic factors. Emerging evidence suggests that dysregulation of circadian rhythms may contribute to the increased cardiovascular risk observed in individuals with obesity. The circadian system, governed by the central pacemaker in the suprachiasmatic nucleus (SCN) of the hypothalamus, orchestrates physiological processes in synchrony with the 24-hour light-dark cycle. Disruption of circadian rhythms, often observed in shift workers and individuals with irregular sleep-wake patterns, has been linked to adverse cardiovascular outcomes. In obesity, alterations in circadian rhythms manifest as disturbances in sleep-wake cycles, meal timing, and hormonal secretion, contributing to metabolic dysfunction and endothelial dysfunction. The key circadian clock genes, including <i>PER1</i>, <i>PER2</i>, <i>PER3</i>, <i>CLOCK</i>, and <i>BMAL1</i>, regulate the rhythmic expression of genes involved in lipid metabolism, glucose homeostasis, and vascular function. Therapeutic interventions targeting circadian rhythms, such as timed feeding, light exposure, and pharmacological modulators of clock gene expression, hold promise for mitigating cardiovascular risk in obesity. This comprehensive review highlights the intricate interplay between circadian mechanisms and cardiovascular risk in obesity.