Smoking and Atherosclerosis: Mechanisms of Disease and New Therapeutic Approaches

Abstract

It has been clear that at least 1 billion adults worldwide are smokers and at least 700 million children are passive smokers at home. Smoking exerts a detrimental effect to many organ systems and is responsible for illnesses such as lung cancer, pneumonia, chronic obstructive pulmonary disease, cancer of head and neck, cancer of the urinary and gastrointestinal tract, periodontal disease, cataract and arthritis. Additionally, smoking is an important modifiable risk factor for the development of cardiovascular disease such as coronary artery disease, stable angina, acute coronary syndromes, sudden death, stroke, peripheral vascular disease, congestive heart failure, erectile dysfunction and aortic aneurysms via initiation and progression of atherosclerosis. A variety of studies has proved that cigarette smoking induces oxidative stress, vascular inflammation, platelet coagulation, vascular dysfunction and impairs serum lipid pro-file in both current and chronic smokers, active and passive smokers and results in detrimental effects on the cardiovascular system. The aim of this review is to depict the physical and biochemical properties of cigarette smoke and, furthermore, elucidate the main pathophysiological mechanisms of cigarette-induced atherosclerosis and overview the new therapeutic approaches for smoking cessation and augmentation of cardiovascular health.

Klotho ameliorates oxidized low density lipoprotein (ox-LDL)-induced oxidative stress via regulating LOX-1 and PI3K/Akt/eNOS pathways

“…Similarly, some natural compounds also protect endothelial cells from ox-LDL-induced apoptosis by modulating the PI3K/Akt/eNOS pathway [44]. In contrast, many studies indicated that decreased NO is another key mechanism underlying endothelial dysfunction, which is interrelated with decreased expression of the Klotho gene [33, 45–47]. In addition, it has been proven that Klotho protects the cardiovascular system through endothelium-derived NO production by humoral pathways [47].…”

Extracellular vesicles released in response to respiratory exposures: implications for chronic disease

“…Further, these diseases share chronic inflammation and oxidative stress as common hallmarks (Barua, Sharma, and Dileepan 2015;Crotty Alexander, Shin, and Hwang 2015;Kelly and Fussell 2015;Siasos et al 2014;Valavanidis et al 2013), suggesting some overlap in the biological processes underlying disease development. Extracellular vesicles (EV) are secreted signaling entities whose production is modulated by pro-inflammatory and oxidative stimuli in vitro.…”

Oral cavity infections: why should cardiologists care about them?

“…One manifestation of this is an increase in plasma concentration of natriuretic peptides, which have a significant diagnostic and prognostic meaning in CHF. The basic natriuretic peptide with a recognised role in diagnostics as well as in monitoring the treatment of CHF patients is plasma concentration of N-terminal pro-B-type natriuretic peptide (NT-proBNP) [37,[39][40][41][42][43][44][45][46].…”