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

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.

Automated summary

Tobacco smoking is a major risk factor for both COPD and ASCVD, and they have common pathogenesis and mutual influence on clinical presentation and prognosis. Smoking-induced systemic inflammation, impaired endothelial function, and oxidative stress play crucial roles in the development and progression of both diseases. Components present in tobacco smoke have adverse effects on various cellular functions, and smoking may also impair the innate immune system and promote oxidative stress in respiratory and vascular systems. This review discusses the importance of smoking in the mechanisms underlying the comorbidity of COPD and ASCVD.