Cigarette Smoking and Adipose Tissue: The Emerging Role in Progression of Atherosclerosis

Abstract

Smoking is an established risk factor for atherosclerosis through several underlying pathways. Moreover, in the development of atherosclerotic plaque formation, obesity, defined as excess fat mass accumulation, also plays a vital role in dyslipidemia and insulin resistance. Substantial evidence shows that cigarette smoking induces multiple pathological effects in adipose tissue, such as differentiation of adipocytes, lipolysis, and secretion properties in adipose tissue. Therefore, there is an emerging speculation in which adipose tissue abnormality induced by smoking or nicotine is likely to accelerate the progression of atherosclerosis. Herein, this review aims to investigate the possible interplay between smoking and adipose tissue dysfunction in the development of atherosclerosis.

Figure 1

Smoking-associated inflammatory response in artery walls. Smoking causes endothelial dysfunction with VSMCs phenotypic modulation. In addition, more macrophages are recruited and activated to secrete cytokines and chemokines. The resultant inflammatory response leads to atherosclerotic plaque formation and subsequent plaque rupture. TNF-α: tumor necrosis factor-α; IL-1, interleukin-1.

Figure 2

The direct effects of smoking on adipocytes. Smoking has direct actions on the differentiation of adipocytes. On the other hand, smoking can promote the release of FFAs through HSL. In turn, increased FFAs can stimulate macrophages to produce more TNF-α, which further induces adipocytes to secrete various kinds of adipokines, such as ICAM-1, IL-6, and leptin. In the above process, several products (FFAs and adipokines) can influence the artery walls. PPAR-γ, peroxisome proliferator activated receptor-γ; HSL, hormone-sensitive lipase; FFAs, free fatty acid; ICAM-1, intracellular adhesion molecule-1; IL-6, interleukin-6; APN, adiponectin.