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.
Highlights
Cardiovascular diseases (CVDs) are identified as the leading causes of death in many countries, in both developing world and industrialized regions [1], and these diseases include coronary artery diseases, ischemic stroke, and peripheral artery diseases
Inflammatory cells are subsequently recruited to the arterial wall, such as monocytes, which differentiate into macrophages and are, as a result, activated to engulf oxidized low-density lipoprotein (LDL) via scavenger receptors, creating foam cells, which secrete chemokines and other kinds of cytokines that further create a vicious cycle, more immune cell infiltration, and activation [13]
perivascular adipose tissue (PVAT) has been reported to produce a wide range of adipokines, similar to visceral adipose tissue to interact with correspondent intima and meditate the vascular inflammation
Summary
Cardiovascular diseases (CVDs) are identified as the leading causes of death in many countries, in both developing world and industrialized regions [1], and these diseases include coronary artery diseases, ischemic stroke, and peripheral artery diseases. Obesity, characterized as excessive adipose tissue, has a harmful effect on vascular function, and its associated comorbidities are prone to develop CVDs. Similar to smoking, obesity in childhood/. A burgeoning body of studies has reported that cigarette smoking has a complicated effect on body weight and the function of adipose tissue [8,9,10]. This specific interaction between cigarette smoking and adipose tissue in atherogenesis may represent a crucial target for future therapy. The objective of the present paper is to delineate the mechanisms through which exposure to chemicals in cigarette smoking affects the differentiated status and functions of adipocytes, which may contribute to AS
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