Exposure to ambient air pollution is one of the leading causes of death world-wide and has been associated with increases in the risk of cardiovascular disease (CVD) and type 2 diabetes (T2D). Nevertheless, the pathophysiology underlying these health effects remains elusive. Our recent research showed that in mice exposure to air pollution, particularly to fine particulate matter (PM_2.5) induces vascular inflammation, impairs vascular signaling in response to VEGF and insulin, interferes with the mobilization of endothelial progenitor cells (EPCs), and exacerbates the metabolic effects of diet-induced obesity and light-induced circadian dysysnchrony.

Our ongoing research aims to determine:

§  How air pollution exposure induces inflammation and insulin resistance in the blood vessels.

§  How air pollution exposure and diet-induced obesity affect EPC homeostasis and function.

§  How these vascular effects contribute to the development and progression of T2D and CVD.

§  How susceptible states such as diet-induced obesity, circadian dyssynchrony, or aging imapct the toxicity of air pollution.

Mission:

We aim to improve public health by understanding how exposure to polluted air induces vascular and cardiometabolic injury in healthy and susceptible individuals.