Mitochondrial Dysfunction Unravels the Potential Molecular Link Between Night Shift Work-Related Circadian Disruption and Elevated Blood Pressure in Human and Mouse Models.

This study demonstrates that circadian rhythm disruption induced by night-shift work is associated with elevated blood pressure in both murine models and human subjects. By integrating rodent and human epidemiological data, we identify mitochondrial dysfunction as the principal mechanistic contributor to this relationship. In mice, data were obtained at 4 and 10 weeks, with sampling performed at both ZT0 and ZT12. Simulated night shift work elevates blood pressure, induces circadian gene dysregulation (e.g., PER1, BMAL1), and precipitates mitochondrial dysfunction and oxidative stress. These findings are corroborated in human night shift workers, where exposure duration is quantitatively associated with increased systolic and diastolic blood pressure and concomitant dysregulation of circadian and mitochondrial markers. Furthermore, the expression levels of these markers correlate with both night shift work exposure and blood pressure. Collectively, the results establish mitochondrial dysfunction as a critical pathway linking circadian disruption to an elevated blood-pressure phenotype, offering new insights into the cardiovascular consequences of shift work.