机构:[1]First Peoples Hosp, Resp Dept 2, Kunming, Yunnan, Peoples R China[2]Tianjin Haihe Hosp, Tianjin, Peoples R China[3]Tianjin Med Univ, Resp Dept, Gen Hosp, Tianjin 300052, Peoples R China[4]Duke Univ, Med Ctr, Div Pulm & Crit Care Med, Durham, NC USA[5]Tianjin Haihe Hosp, Resp Dept, Tianjin, Peoples R China
Background: Obstructive sleep apnea (OSA) occurs in 4% of middle-aged men and 2% of middle-aged women in the general population, and the prevalence is even higher in specific patient groups. OSA is an independent risk factor for a variety of cardiovascular diseases. Endothelial injury could be the pivotal determinant in the development of cardiovascular pathology in OSA. Endothelial damage ultimately represents a dynamic balance between the magnitude of injury and the capacity for repair. Bone marrow-derived endothelial progenitor cells (EPCs) within adult peripheral blood present a possible means of vascular maintenance that could home to sites of injury and restore endothelial integrity and normal function. Methods: We summarized pathogenetic mechanisms of OSA and searched for available studies on numbers and functions of EPCs in patients with OSA to explore the potential links between the numbers and functions of EPCs and OSA. In particular, we tried to elucidate the molecular mechanisms of the effects of OSA on EPCs. Conclusion: Intermittent hypoxia cycles and sleep fragmentation are major pathophysiologic characters of OSA. Intermittent hypoxia acts as a trigger of oxidative stress, systemic inflammation, and sympathetic activation. Sleep fragmentation is associated with a burst of sympathetic activation and systemic inflammation. In most studies, a reduction in circulating EPCs has emerged. The possible mechanisms underlying the decrease in the number or function of EPCs include prolonged inflammation response, oxidative stress, increased sympathetic activation, physiological adaptive responses of tissue to hypoxia, reduced EPC mobilization, EPC apoptosis, and functional impairment in untreated OSA. Continuous positive airway pressure (CPAP) therapy for OSA affects the mobilization, apoptosis, and function of EPCs through preventing intermittent hypoxia episodes, improving sleep quality, and reducing systemic inflammation, oxidative stress levels, and sympathetic overactivation. To improve CPAP adherence, the medical staff should pay attention to making the titration trial a comfortable first CPAP experience for the patients; for example, using the most appropriate ventilators or proper humidification. It is also important to give the patients education and support about CPAP use in the follow-up, especially in the early stage of the treatment.
基金:
National Natural Science Foundation of China [81270144, 30800507, 81170071]
第一作者机构:[1]First Peoples Hosp, Resp Dept 2, Kunming, Yunnan, Peoples R China
共同第一作者:
通讯作者:
通讯机构:[3]Tianjin Med Univ, Resp Dept, Gen Hosp, Tianjin 300052, Peoples R China[4]Duke Univ, Med Ctr, Div Pulm & Crit Care Med, Durham, NC USA[5]Tianjin Haihe Hosp, Resp Dept, Tianjin, Peoples R China[*1]Respiratory Department of Tianjin Medical University General Hospital, Tianjin 300052, People’s Republic of China[*2]Respiratory Department of Tianjin Haihe Hospital, Tianjin 300350, People’s Republic of China
推荐引用方式(GB/T 7714):
Wang Qing,Wu Qi,Feng Jing,et al.Obstructive sleep apnea and endothelial progenitor cells[J].PATIENT PREFERENCE AND ADHERENCE.2013,7:1077-1090.doi:10.2147/PPA.S51562.
APA:
Wang, Qing,Wu, Qi,Feng, Jing&Sun, Xin.(2013).Obstructive sleep apnea and endothelial progenitor cells.PATIENT PREFERENCE AND ADHERENCE,7,
MLA:
Wang, Qing,et al."Obstructive sleep apnea and endothelial progenitor cells".PATIENT PREFERENCE AND ADHERENCE 7.(2013):1077-1090