论文部分内容阅读
阻塞型睡眠呼吸暂停综合征(obstructive sleep apnea syndrome,OSAS)是临床上常见的重要慢性睡眠呼吸疾病。近年来的研究已证实,OSAS是动脉粥样硬化性疾病的独立危险因素。OSAS患者在睡眠时由于上气道阻塞或部分阻塞导致反复发作的慢性间歇性缺氧,这可能是其诱发动脉粥样硬化性疾病的重要原因,此过程中可能的分子机制包括:I-κB复合物和P38激酶激活调控NF-κB信号通路;端粒酶和Fas死亡配体依赖性细胞凋亡调控途径;间歇性缺氧诱发肝脏损伤导致高胆固醇血症和脂质过氧化反应代谢紊乱,引起不可逆的血管和周围组织重塑,伴有平滑肌增生和纤维化,导致动脉粥样硬化。
Obstructive sleep apnea syndrome (OSAS) is a clinically important chronic sleep-respiratory disease. Recent studies have confirmed that OSAS is an independent risk factor for atherosclerotic disease. OSAS patients with recurrent chronic intermittent hypoxia during sleep obstruction due to obstruction or upper airway obstruction, which may be caused by atherosclerotic disease is an important reason, the possible molecular mechanisms in this process include: I-κB Complex and P38 kinase activation regulate NF-κB signaling pathway; telomerase and Fas ligand-dependent apoptosis pathway; intermittent hypoxia-induced liver injury lead to hypercholesterolemia and lipid peroxidation metabolic disorders, Irreversible vascular and surrounding tissue remodeling, with smooth muscle proliferation and fibrosis, leading to atherosclerosis.