Cigarette Smoking and Adipose Tissue: The Emerging Role in Progression 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.