Department of Medicine, The University of Hong Kong, Queen Mary Hospital, Hong Kong, China.
Respirology. 2013 Jan;18(1):39-46. doi: 10.1111/j.1440-1843.2012.02212.x.
The endothelium functions not only as a semi-selective barrier between body tissue and circulation; it also plays an active role in the maintenance of a healthy vasculature. Endothelial dysfunction is increasingly found to play a pivotal role in the pathogenesis of atherosclerosis. Impaired endothelium-dependent vasodilation, as a marker of endothelial dysfunction, predates and predicts cardiovascular disease. Endothelial dysfunction is thought to result from oxidative stress, inflammatory gene activation and cytokine cascade, as well as impairment of endothelial repair mechanisms. In the context of sleep-related breathing disorders, obstructive sleep apnoea (OSA) is postulated to contribute independently to cardiovascular morbidity and mortality. Thus, endothelial dysfunction is an important target of research in vascular pathogenesis and also serves as an intermediary outcome indicator in clinical trials evaluating cardiovascular sequelae in OSA. Basic or translational studies have identified cellular and molecular mechanisms of potential relevance to endothelial dysfunction in OSA, while epidemiological or clinical studies have shown endothelial dysfunction attributable to sleep-disordered breathing, which could improve with effective treatment of OSA. Endothelial dysfunction is poised to serve as a call for timely intervention with possibility of halting or even reverting vascular injury in sleep-related breathing disorders. Much remains to be explored about the complex pathways of endothelial dysfunction and its clinical manifestations in subjects with OSA, which are likely to involve multiple contributing factors. Evidence-based information will allow us to construct the framework for guiding individualized clinical management and public health strategies for OSA, as well as cardiometabolic diseases.
内皮细胞不仅作为身体组织和循环之间的半选择性屏障发挥作用，而且在维持健康的血管方面也发挥着积极的作用。内皮功能障碍越来越被认为在动脉粥样硬化的发病机制中起关键作用。受损的内皮依赖性血管舒张作为内皮功能障碍的标志物，先于并预测心血管疾病。内皮功能障碍被认为是由于氧化应激、炎症基因激活和细胞因子级联反应以及内皮修复机制受损所致。在与睡眠相关的呼吸障碍的背景下，阻塞性睡眠呼吸暂停（OSA）被认为独立地导致心血管发病率和死亡率。因此，内皮功能障碍是血管发病机制研究的重要靶点，也是评估 OSA 心血管后果的临床试验中的中介结果指标。基础或转化研究已经确定了与 OSA 中内皮功能障碍相关的细胞和分子机制，而流行病学或临床研究表明，与睡眠呼吸障碍相关的内皮功能障碍可以通过 OSA 的有效治疗得到改善。内皮功能障碍可能成为及时干预的信号，有可能阻止甚至逆转与睡眠相关的呼吸障碍中的血管损伤。关于 OSA 患者内皮功能障碍及其临床表现的复杂途径仍有许多需要探索，这可能涉及多个相关因素。基于证据的信息将使我们能够构建指导 OSA 以及心脏代谢疾病个体化临床管理和公共卫生策略的框架。
