Abstract
Smoking is one of the most important preventable factors causing peripheral artery disease (PAD). The purpose of this review is to comprehensively analyze and summarize the pathogenesis and clinical characteristics of smoking in PAD based on existing clinical, in vivo, and in vitro studies. Extensive searches and literature reviews have shown that a large amount of data exists on the pathological process underlying the effects of cigarette smoke and its components on PAD through various mechanisms. Cigarette smoke extracts (CSE) induce endothelial cell dysfunction, smooth muscle cell remodeling and macrophage phenotypic transformation through multiple molecular mechanisms. These pathological changes are the molecular basis for the occurrence and development of peripheral vascular diseases. With few discussions on the topic, we will summarize recent insights into the effect of smoking on regulating PAD through multiple pathways and its possible pathogenic mechanism.
Highlights
With changes in global population epidemiology, the incidence of PAD may increase in the future [1]
Many factors promote the development of this disease, and smoking is an independent risk factor for PAD
Numerous studies confirm the association between smoking and cardiovascular disease
Summary
With changes in global population epidemiology, the incidence of PAD may increase in the future [1]. Various studies have shown that for long-term smokers, whether they are active smokers or passive smokers, harmful substances may induce various phenotypic changes and dysfunction of macrophages, endothelial cells and smooth muscle cells through various mechanisms, promoting the occurrence and development of vascular diseases [34, 35] (Figure 2). Cigarette smoke can increase the expression of ETB receptor in endothelial cells, and cause endothelial dysfunction and contraction of VSMCs through the effect of ET-1 and the reduction of NO synthesis [66, 121, 124]. Activate Rho kinase and promote phosphorylation of eNOS (Thr113), thereby inhibiting the production of NO in ECs. Increased expression of ETB receptors causes endothelial dysfunction through the action of ET-1. Inactivating protein-1α by cleaving serpins at an inhibitory site region, which will induce the expression of proinflammatory molecules
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