Chronodisruption induced by artificial light exposure: Unraveling its molecular pathways and impacts on cardiometabolic dysfunctions

Abstract

Chronodisruption, defined as misalignment between endogenous circadian rhythms and external environmental cues, is increasingly implicated in cardiometabolic dysfunction, which elevates cardiovascular disease risk. Artificial light exposure, particularly during nighttime, disrupts the circadian clock by altering molecular pathways involving clock genes, melatonin secretion, and metabolic regulators. Animal studies have revealed that such disruptions exacerbate insulin resistance, dyslipidemia, and systemic inflammation—key risk factors for cardiovascular disease. Evidence also suggests impaired autonomic regulation, endothelial dysfunction, and altered myocardial metabolism due to circadian misalignment. Artificial light also alters other indices of cardiovascular function by raising blood pressure and the atherogenic index, both of which have been shown to hamper recovery from vascular and cardiovascular diseases. Despite these advances, knowledge gaps remain, including species-specific differences, long-term effects of varying light intensities, durations, and spectra, and translational applicability to humans. This review aims to elucidate several molecular pathways responsible for this disruption, and to examine how they interfere with physiological systems using animal studies and how they translate into clinical contexts. Bridging these gaps could inform novel preventive and therapeutic strategies targeting chronodisruption-induced cardiometabolic risks.