Breaking barriers in obstructive sleep apnea. Focus on "Intermittent hypoxia-induced endothelial barrier dysfunction requires ROS-dependent MAP kinase activation".
Breaking barriers in obstructive sleep apnea. Focus on "Intermittent hypoxia-induced endothelial barrier dysfunction requires ROS-dependent MAP kinase activation".
复制标题
打破阻塞性睡眠呼吸暂停的障碍。
DOI：
10.1152/ajpcell.00072.2014
复制
发表时间：
2014
期刊：
影响因子：
--
通讯作者：
Yuan,JasonX-J
中科院分区：
文献类型：
--
作者：
Smith,KimberlyA;Yuan,JasonX-J
影响我们社会的更常见的健康问题之一是阻塞性睡眠呼吸暂停 (OSA)，它影响至少 10% 的总人口，主要是超重或肥胖的男性 (12)。 OSA 被定义为由于睡眠期间气道阻塞或气道阻力增加而导致咽部气道反复、间歇性塌陷而导致的呼吸停止，由于其普遍性和严重后果，它是一个众所周知的公共卫生问题。 OSA 最常见的症状是早晨疲劳、白天嗜睡、夜间利尿引起的觉醒和频繁打鼾，但许多患者通过改变生活方式来补偿，症状很少或不存在。 OSA 是通过多导睡眠图进行睡眠评估后诊断的，其中包括同时记录睡眠、气流、呼吸努力、氧饱和度和大脑活动。 OSA 的后果包括神经认知障碍和心血管疾病，包括高血压、中风、冠状动脉疾病和心力衰竭 (7)。此外，多项研究表明 OSA 与肺水肿 (4) 和肺动脉高压 (10) 相关。大量患有心脏疾病并伴有 OSA 的患者并未报告白天过度嗜睡，因此不考虑进行 OSA 的诊断性睡眠评估和治疗。众所周知，未经治疗的 OSA 会导致心血管疾病进展并增加死亡率。反复呼吸暂停会导致慢性间歇性缺氧 (CIH)，这是 OSA 的一个标志。大鼠和小鼠暴露于 CIH 3 至 5 周足以诱发与 OSA 患者相似的病理变化，例如内皮功能障碍、动脉粥样硬化、全身性高血压、肺动脉高压和心力衰竭 (3)。有人认为颈动脉体构成了检测与呼吸暂停相关的全身性缺氧的前线防御系统 (2)。 CIH 对颈动脉体产生的两个主要影响是对急性缺氧的增强反应和颈动脉体的持久激活，这种激活在 CIH 终止后持续数小时 (9)。有人提出，CIH 引起的颈动脉体反应增强的病理效应是由于活性氧 (ROS) 增加所致 (8)。 CIH 通过促氧化剂上调和抗氧化剂下调导致 ROS 增加 (6)。 ROS是在正常细胞代谢或分子氧不完全还原过程中产生的一组高度不稳定的分子。这些物种参与生长和分化等基本细胞活动的调节，然而，ROS 的过量产生会导致氧化应激并造成严重损伤 (11)。暴露于 CIH 的小鼠和大鼠的颈动脉体、肾上腺髓质和中枢神经系统中的 ROS 升高，导致
ONE OF THE MORE COMMON HEALTH issues affecting our society is obstructive sleep apnea (OSA), which affects at least 10% of the general population, primarily overweight or obese men (12). OSA, defined as the cessation of breathing caused by the repetitive, episodic collapse of the pharyngeal airway due to an airway obstruction or increased airway resistance during sleep, is a well-known public health problem due to its prevalence and the severe consequences of this disorder. The most common symptoms of OSA are morning fatigue, increased daytime sleepiness, arousals with nocturnal diuresis, and frequent snoring, yet many patients present with minimal or absent symptoms by compensating with lifestyle modifications. OSA is diagnosed following a sleep evaluation with polysomnography, which involves simultaneous recording of sleep, air flow, respiratory effort, oxygen saturation, and brain activity. The consequences of OSA include neurocognitive impairment and cardiovascular morbidities including hypertension, stroke, coronary artery disease, and heart failure (7). Additionally, several studies have shown OSA to be associated with pulmonary edema (4) and pulmonary hypertension (10). A substantial number of patients with cardiac disorders and concomitant OSA do not report excessive daytime sleepiness and are therefore not considered for diagnostic sleep evaluation and treatment for OSA. It is well understood that untreated OSA can lead to the progression of cardiovascular disease and increased mortality.Recurrent apneas result in chronic intermittent hypoxia (CIH), a hallmark of OSA. Exposure of rats and mice to CIH for 3 to 5 weeks is sufficient to induce pathological changes similar to those seen in OSA patients, such as endothelial dysfunction, atherosclerosis, systemic hypertension, pulmonary hypertension, and heart failure (3). It has been suggested that the carotid bodies constitute the frontline defense system for detecting systemic hypoxia associated with apneas (2). The two major effects exerted by CIH on the carotid body are augmented response to acute hypoxia and long-lasting activation of the carotid body, which persist for several hours after termination of CIH (9). It has been proposed that the pathological effects of CIH-induced augmented carotid body responses are due to increased reactive oxygen species (ROS)(8). CIH results in increased ROS by both upregulation of pro-oxidants and downregulation of anti-oxidants (6). ROS are a group of highly unstable molecules generated during normal cellular metabolism or during incomplete reduction of molecular oxygen. These species are involved in the regulation of fundamental cellular activities such as growth and differentiation, however, overproduction of ROS results in oxidative stress and causes significant injury (11). Mice and rats exposed to CIH display elevated ROS in the carotid body, adrenal medulla, and central nervous system resulting in increased
反应溅射非晶 Ta--Si--N 薄膜的分解与纳米晶化
影响因子：
3.2
作者：
C. Pinnow;M. Bicker;U. Geyer;S. Schneider;G. Goerigk
通讯作者：
G. Goerigk
影响因子：
5.5
作者：
Makarenko, Vladislav V.;Usatyuk, Peter V.;Prabhakar, Nanduri R.
通讯作者：
Prabhakar, Nanduri R.