Abstract
Atherosclerosis has been identified as a chronic inflammatory disease of the arterial vessel wall. Accumulating evidence indicates that different cells from the tunica intima, media, adventitia, and perivascular adipose tissue not only comprise the intact and normal arterial vessel wall but also participate all in the inflammatory response of atherosclerosis via multiple intricate pathways. For instance, endothelial dysfunction has historically been considered to be the initiator of the development of atherosclerosis. The migration and proliferation of smooth muscle cells also play a pivotal role in the progression of atherosclerosis. Additionally, the fibroblasts from the adventitia and adipocytes from perivascular adipose tissue have received considerable attention given their special functions that contribute to atherosclerosis. In addition, numerous types of cytokines produced by different cells from the arterial vessel wall, including endothelium-derived relaxing factors, endothelium-derived contracting factors, tumor necrosis factors, interleukin, adhesion molecules, interferon, and adventitium-derived relaxing factors, have been implicated in atherosclerosis. Herein, we summarize the possible roles of different cells from the entire arterial vessel wall in the pathogenesis of atherosclerosis.
Highlights
As a major public health issue, atherosclerosis in concert with its related disorders, such as coronary heart diseases, stroke, and peripheral vascular diseases, has been the leading cause of mortality and morbidity worldwide [1, 2]
The new paradigm of an “outside to inside” hypothesis is supported by compelling evidence [11, 12], which predominantly uncovers the functional significance of the tunica intima, adventitia, and perivascular adipose tissue
This review will shed light on different cells, including endothelial cells (ECs), smooth muscle cells (SMCs), fibroblasts, and adipocytes from the tunica intima, media, adventitia, and PVAT and their related cytokines, and elucidate how these cells contribute to the pathogenesis of atherosclerosis (Figure 1)
Summary
As a major public health issue, atherosclerosis in concert with its related disorders, such as coronary heart diseases, stroke, and peripheral vascular diseases, has been the leading cause of mortality and morbidity worldwide [1, 2]. Some of the pioneers have unceasingly devoted themselves to investigate the possible mechanisms implicated in the pathogenesis of atherosclerosis and have made considerable progress, such as the “response to inflammation” theory based on “response to injury” theory [3] and “response to lipoprotein retention” hypothesis [4,5,6]. Classical doctrine indicates that smooth muscle cells (SMCs) predominantly from the medial have a crucial impact on the development of atherosclerosis based on their migration into the intima and proliferation [13]. This review will shed light on different cells, including endothelial cells (ECs), SMCs, fibroblasts, and adipocytes from the tunica intima, media, adventitia, and PVAT and their related cytokines, and elucidate how these cells contribute to the pathogenesis of atherosclerosis (Figure 1)
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