Coronary atherosclerosis (CAS), a leading cause of cardiovascular disease, is a major cause of death worldwide. CAS is a chronic disease in the aorta that can be caused by dyslipidemia, abnormal glucose metabolism, endothelial cell dysfunction, vascular smooth muscle cell (VSMC) or fibrous connective tissue hyperplasia, immune inflammatory reactions, and many other factors. The pathogenesis of CAS is not fully understood, as it is a complex lesion complicated by multiple factors. Damage-response theories have put forward endothelial cell (EC) injury as the initiating factor for CAS; the addition of lipid metabolism disorders may enhance monocyte adhesion, increase the proliferation and migration of fibroblasts and VSMCs, and accelerate the development of CAS. Furthermore, inflammatory and immune responses can create a vicious cycle of endothelial injury, which also plays key roles in the formation of CAS. Therefore, in order to elucidate the mechanisms controlling CAS, it is important to study the etiology of vascular cell dysfunction, abnormal energy and metabolism disorders, and immune and inflammatory reactions. Non-coding RNAs play regulatory roles in the pathogenesis of CAS, especially long non-coding RNAs (lncRNAs); lncRNAs have recently become a major focus for cardiovascular disease mechanisms, as they play numerous roles in the progression of CAS. Therefore, in this review, we discuss the role of lncRNAs in the pathogenesis of coronary CAS, and their role in the prevention and treatment of coronary CAS.
Keywords: Cellular dysfunction; Coronary atherosclerosis; Immune inflammatory response; LncRNAs; Metabolic disorders.
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