The Role of Smoking in the Mechanisms of Development of Chronic Obstructive Pulmonary Disease and Atherosclerosis

Abstract

Tobacco smoking is a major cause of chronic obstructive pulmonary disease (COPD) and atherosclerotic cardiovascular disease (ASCVD). These diseases share common pathogenesis and significantly influence each other's clinical presentation and prognosis. There is increasing evidence that the mechanisms underlying the comorbidity of COPD and ASCVD are complex and multifactorial. Smoking-induced systemic inflammation, impaired endothelial function and oxidative stress may contribute to the development and progression of both diseases. The components present in tobacco smoke can have adverse effects on various cellular functions, including macrophages and endothelial cells. Smoking may also affect the innate immune system, impair apoptosis, and promote oxidative stress in the respiratory and vascular systems. The purpose of this review is to discuss the importance of smoking in the mechanisms underlying the comorbid course of COPD and ASCVD.

Keywords: COPD; atherosclerosis; cigarette smoking; comorbidity; innate immune system; oxidative stress; tobacco smoking.

Figure 1

Involvement of components of tobacco smoke in the activation of proinflammatory mechanisms. Abbreviations: ABCA1—ATP binding cassette subfamily A member 1, eNOS—endothelial nitric oxide synthase, IL-1β—interleukin-1 beta, ICAM-1—intercellular adhesion molecule 1, iNOS—inducible nitric oxide synthase, KLF4—Kruppel-like factor 4, NLRP3—NLR family pyrin domain containing 3, NO—nitric oxide, TLR4—Toll-like receptor 4, VCAM-1—vascular cell adhesion molecule 1.

Figure 2

Mechanisms of emphysema development in smoking. Abbreviations: ABCA1—ATP binding cassette subfamily A member 1, CXCL—chemokine (C-X-C motif) ligand, eNOS—endothelial nitric oxide synthase, iNOS—inducible nitric oxide synthase, IL-1β—interleukin-1 beta, MMP—matrix metalloproteinases, NE—neutrophil elastase, NLRP3—NLR family pyrin domain containing 3, nNOS—neuronal nitric oxides synthase, TLR4—Toll-like receptor 4, VEGF—vascular endothelial growth factor, VEGFR2—vascular endothelial growth factor receptor 2.

Figure 3

Effect of smoking on the common links in the pathogenesis of COPD and atherosclerotic cardiovascular diseases.