Tobacco smoking is the single most preventable risk factor related to the development of cardiovascular disease. It was demonstrated that tobacco smoke contains a thousand compounds potentially harmful to human health. As tobacco use declined over time, electronic cigarettes were introduced as an alternative. E-cigarettes are a modern and technological surrogate of traditional cigarettes and use heat to convert a nicotine solution or a flavored nicotine-free solution into vapor. Even though all the ingredients contained in the liquid of E-cigarettes are approved as food additives, the harmlessness of these electronic devices is still not fully proven in humans. The general mechanisms by which smoking results in cardiovascular events include the development of atherosclerotic changes with a hypercoagulable state and an increased risk of thrombosis. Endothelial dysfunction has been recognized as a hallmark of preclinical systemic atherosclerosis and as a useful marker to stratify the risk of cardiovascular disease. Based on these considerations, in this chapter, we (1) discussed the role of endothelial dysfunction and its contributing factors, such as oxidative stress and inflammation, in the development of cardiovascular diseases and (2) reported the studies which investigated the effect of tobacco and electronic smoking on the biomarkers of endothelial dysfunction, oxidative stress, and inflammation.
Part of the book: Smoking Prevention and Cessation
Basic and translational research on lung biology and pathology can greatly benefit from the development of 3D in vitro models with physiological relevance. Lung organoids and lungs-on-chip allow the creation of different kinds of in vitro microenvironments, that can be useful for the elucidation of novel pathogenetic pathways, for example concerning tissue fibrosis in chronic diseases. Moreover, they represent important translational models for the identification of novel therapeutic targets, and for preliminary testing of new drugs. In this chapter, we provide a selected overview of recent studies on innovative 3D in vitro models that have enhanced our knowledge on chronic obstructive pulmonary disease (COPD) and idiopathic pulmonary fibrosis (IPF), particularly concerning oxidative stress and pro-fibrotic pathogenetic mechanisms. Despite several limitations, these complex models must be considered as complementary in all respects to in vivo studies on animal models and clinical research.
Part of the book: Cell Interaction