Takeda Yoshinori, Kimura Fuminori, Takasawa Shin
Department of Biochemistry, Nara Medical University, 840 Shijo-cho, Kashihara 634-8521, Japan.
Department of Obstetrics and Gynecology, Nara Medical University, 840 Shijo-cho, Kashihara 634-8522, Japan.
Life (Basel). 2024 Jan 22;14(1):157. doi: 10.3390/life14010157.
Intermittent hypoxia (IH) is a central characteristic of sleep apnea syndrome (SAS), and it subjects cells in the body to repetitive apnea, chronic hypoxia, oxygen desaturation, and hypercapnia. Since SAS is linked to various serious cardiovascular complications, especially hypertension, many studies have been conducted to elucidate the mechanism of hypertension induced by SAS/IH. Hypertension in SAS is associated with numerous cardiovascular disorders. As hypertension is the most common complication of SAS, cell and animal models to study SAS/IH have developed and provided lots of hints for elucidating the molecular mechanisms of hypertension induced by IH. However, the detailed mechanisms are obscure and under investigation. This review outlines the molecular mechanisms of hypertension in IH, which include the regulation systems of reactive oxygen species (ROS) that activate the renin-angiotensin system (RAS) and catecholamine biosynthesis in the sympathetic nervous system, resulting in hypertension. And hypoxia-inducible factors (HIFs), Endotheline 1 (ET-1), and inflammatory factors are also mentioned. In addition, we will discuss the influences of SAS/IH in cardiovascular dysfunction and the relationship of microRNA (miRNA)s to regulate the key molecules in each mechanism, which has become more apparent in recent years. These findings provide insight into the pathogenesis of SAS and help in the development of future treatments.
间歇性缺氧（IH）是睡眠呼吸暂停综合征（SAS）的核心特征，它使体内细胞反复经历呼吸暂停、慢性缺氧、氧饱和度降低和高碳酸血症。由于SAS与各种严重的心血管并发症相关，尤其是高血压，因此已经进行了许多研究来阐明SAS/IH诱发高血压的机制。SAS中的高血压与多种心血管疾病有关。由于高血压是SAS最常见的并发症，用于研究SAS/IH的细胞和动物模型已经建立，并为阐明IH诱发高血压的分子机制提供了许多线索。然而，具体机制尚不清楚，仍在研究中。本综述概述了IH中高血压的分子机制，其中包括激活肾素-血管紧张素系统（RAS）的活性氧（ROS）调节系统以及交感神经系统中儿茶酚胺的生物合成，从而导致高血压。此外，还提到了缺氧诱导因子（HIFs）、内皮素1（ET-1）和炎症因子。此外，我们将讨论SAS/IH对心血管功能障碍的影响以及微小RNA（miRNA）与调节每种机制中关键分子的关系，近年来这种关系变得更加明显。这些发现为SAS的发病机制提供了见解，并有助于未来治疗方法的开发。
