Short-term PM2.5 exposure is related to
vascular remodeling and stiffness. Mitochondria-targeted
antioxidant MitoQ is reported to improve the occurrence and development of mitochondrial redox-related diseases. At present, there is limited data on whether
MitoQ can alleviate the vascular damage caused by PM2.5. Therefore, the current study was aimed to evaluate the protective role of
MitoQ on aortic
fibrosis induced by PM2.5 exposure. Vascular Doppler ultrasound manifested PM2.5 damaged both vascular function and structure in C57BL/6J mice. Histopathological analysis found that PM2.5 induced aortic
fibrosis and disordered elastic fibers, accompanied by
collagen I/III deposition and synthetic phenotype remodeling of vascular smooth muscle cells; while these alterations were partially alleviated following
MitoQ treatment. We further demonstrated that
mitochondrial dysfunction, including mitochondrial
reactive oxygen species (ROS) overproduction and activated
superoxide dismutase 2 (SOD2) expression, decreased mitochondrial membrane potential (
MMP), oxygen consumption rate (OCR),
ATP and increased intracellular Ca2+, as well as mitochondrial fragmentation caused by increased Drp1 expression and decreased Mfn2 expression, occurred in PM2.5-exposed aorta or human aortic vascular smooth muscle cells (HAVSMCs), which were reversed by
MitoQ. Moreover, the enhanced expressions of LC3II/I, p62, PINK1 and Parkin regulated mitophagy in PM2.5-exposed aorta and HAVSMCs were weakened by
MitoQ. Transfection with PINK1
siRNA in PM2.5-exposed HAVSMCs further improved the effects of
MitoQ on HAVSMCs synthetic phenotype remodeling, mitochondrial fragmentation and mitophagy. In summary, our data demonstrated that
MitoQ treatment had a protective role in aortic
fibrosis after PM2.5 exposure through mitochondrial quality control, which regulated by mitochondrial ROS/PINK1/Parkin-mediated mitophagy. Our study provides a possible targeted
therapy for PM2.5-induced arterial stiffness.