Our results demonstrate that acute exposure to tobacco smoking as well as electronic cigarettes influences vascular and respiratory function. Where tobacco smoking significantly increased microparticle formation, indicative of possible endothelial injury, electronic cigarettes use induced vasoreactivity and decreased peak expiratory flow. These findings suggest that both electronic cigarettes and tobacco smoking negatively impact vascular function.

±0.28 ischaemic/control limb ratio; n=8, p<0.05) CB-ECFCs into mouse ischaemic hindlimbs inhibited and promoted revascularisation whilst regulating host eNOS-associated angiogenic signalling. Together, these findings indicate a key role for NOX4 in CB-ECFCs, highlighting its potential as a target for enhancing their reparative function through therapeutic priming to support creation of a pro-reparative microenvironment and promotion of effective post ischaemic revascularisation.