The relationship between atherosclerosis and pulmonary emphysema

Abstract

The etiopathogenesis of atherosclerosis and subsequent pulmonary emphysema has not been fully elucidated. Foam cells are of great importance in the development of these diseases. It is known that local cytokine secretion and modification of native lipoprotein particles, which are internalized by the vascular and alveolar macrophages via the scavenger receptors on the surfaces of these cells, lead to the formation of foam cells. Thus, the exacerbation of local inflammatory process in the vascular and lung tissue ensues due to a generation of reactive oxygen species, resulting in further lipoprotein modification and cytokine production. Accumulating evidence suggests that oxidants may facilitate the inflammatory response by impairing antiprotease function, directly attacking vascular and lung matrix proteins and by inactivating enzymes involved in elastin synthesis and vascular and lung repair. Cigarette smoke is recognized as a rich source of oxidants. Nearly 90% of all patients with chronic obstructive pulmonary disease are smokers. The process of atherogenesis is also influenced by tobacco smoke. The role of vascular and alveolar macrophages has become increasingly important in understanding the development of atherosclerosis and resulting pulmonary emphysema.