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although to a lesser degree than standard cigarettes, electronic cigarettes lead to an important increase in soluble nicotinamide adenine dinucleotide phosphate oxidase 2-derived peptides and a concomitant decrease in nitric oxide bioavailability.85 Nonetheless, in human coronary endothelial cells, tobacco smoke, but not electronic cigarette aerosols, was shown to induce nuclear factor erythroid 2-related factor 2 oxidative stress sensing factor transcription.86 In another study, exposure of umbilical endothelial vein cells to electronic cigarette compounds induced cytotoxic pathways, inhibited cell proliferation and altered cellular morphology when compared with regular tobacco.87 An animal study suggested that electronic cigarettes could also hamper metabolic homeostasis

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