Grant: Project Grant

Classical cardiovascular risk factors such as high cholesterol and cigarette smoking are associated with an impairment of neovascularization, the protective growth of new vessels in response to ischemia. However, the precise mechanisms that are involved in that physiopathology remain to be determined. Extracellular vesicles (EVs) are small pouches secreted by cells. They are emerging as key regulators of several physiological and pathophysiological processes. We propose that cardiovascular risk factors involving excessive oxidative stress levels lead to impairment in the capacity of EVs to promote neovascularization. Using a combination of in vitro and in vivo models, our study will identify important novel mechanisms that are involved in the modulation of ischemia-induced neovascularization in pathological conditions. EVs could eventually represent novel therapeutic vectors to improve neovascularisation and restore tissue function in ischemic cardiovascular diseases.