Behavioral Sleep Medicine Program, Department of Psychiatry, Perelman School of Medicine, University of Pennsylvania, PA, USA ; Center for Sleep and Circadian Neurobiology, University of Pennsylvania, PA, USA.
Nat Sci Sleep. 2013 Jul 22;5:93-107. doi: 10.2147/NSS.S31063. Print 2013.
Habitual sleep duration has been associated with cardiometabolic disease, via several mechanistic pathways, but few have been thoroughly explored. One hypothesis is that short and/or long sleep duration is associated with a proinflammatory state, which could increase risk for cardiovascular and metabolic diseases. This hypothesis has been largely explored in the context of experimental sleep deprivation studies which have attempted to demonstrate changes in proinflammatory markers following acute sleep loss in the laboratory. Despite the controlled environment available in these studies, samples tend to lack generalization to the population at large and acute sleep deprivation may not be a perfect analog for short sleep. To address these limitations, population based studies have explored associations between proinflammatory markers and habitual sleep duration. This review summarizes what is known from experimental and cross-sectional studies about the association between sleep duration, cardiovascular disease, and proinflammatory biomarkers. First, the association between sleep duration with both morbidity and mortality, with a focus on cardiovascular disease, is reviewed. Then, a brief review of the potential role of proinflammatory markers in cardiovascular disease is presented. The majority of this review details specific findings related to specific molecules, including tumor necrosis factor-α, interleukins-1, -6, and -17, C-reactive protein, coagulation molecules, cellular adhesion molecules, and visfatin. Finally, a discussion of the limitations of current studies and future directions is provided.
习惯性的睡眠时间与心血管代谢疾病有关，通过几种机制途径，但很少有被彻底探索。一个假设是，短时间和/或长时间的睡眠与促炎状态有关，这可能会增加患心血管和代谢疾病的风险。这个假设在实验性睡眠剥夺研究中得到了广泛的探索，这些研究试图在实验室中证明急性睡眠缺失后促炎标志物的变化。尽管这些研究中可获得受控环境，但样本往往缺乏对总体人群的概括性，并且急性睡眠剥夺可能不是短时间睡眠的完美模拟。为了解决这些限制，基于人群的研究已经探索了促炎标志物与习惯性睡眠时间之间的关联。这篇综述总结了实验和横断面研究中关于睡眠时间、心血管疾病和促炎生物标志物之间关联的已知情况。首先，回顾了睡眠时间与发病率和死亡率之间的关联，重点是心血管疾病。然后，简要回顾了促炎标志物在心血管疾病中的潜在作用。这篇综述的大部分内容详细介绍了与特定分子相关的具体发现，包括肿瘤坏死因子-α、白细胞介素-1、-6 和 -17、C 反应蛋白、凝血分子、细胞黏附分子和内脂素。最后，讨论了当前研究的局限性和未来的方向。
