Combined exposure of sleep deprivation and environmental particulate matter drives aging in multiple systems

Sleep disturbance accelerates aging, with accompanying exposure to air pollution. However, most studies ignore the combined exposure. This study aimed to investigate the combined effects of sleep deprivation and PM2.5 exposure on multi-system aging and to explore the damage mechanisms. The sleep deprivation instrument and the Shanghai Meteorological and Environmental Animal Exposure System (Shanghai-METAS) were used to construct a combined exposure model for one month. Our study used multiple behavioral, imaging, and molecular biological examinations to describe the aging characteristics in the cardiovascular system, metabolism, and central nervous system. Besides, the mechanisms in Sirt1, Wnt10β pathways were explored and correlation of damage among tissues was clarified. Based on sleep disruption, PM2.5 exposure was able to induce elevated serum T-CHO levels, impaired conditioned learning ability, abnormal brain tissue metabolic levels, and aberrant expression of multiple molecular markers related to cellular senescence, whereas PM2.5 exposure alone did not induce changes in the above indices. In addition, the Sirt1, Wnt10β pathway mediated cardiac and hepatic aging induced by combined exposure. Moreover, there was a significant correlation between heart and liver aging damage, which suggesting heart-liver axis may be involved in the aging process. Sleep deprivation and PM2.5 exposure trigger senescence in multiple tissues. In particular, on the basis of sleep deprivation, PM2.5 accelerates of the aging process in several tissues and organs. The problem of air pollution on top of sleep disturbance should be taken seriously, as it has a greater potential to accelerate aging than air pollution.