The role of metalloproteinases in the pathogenesis of Obstructive Sleep Apnea Syndrome

Q4 Medicine
Nataliya Vasilenok, N. Olszewska, E. Olszewska
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引用次数: 0

Abstract

Obstructive Sleep Apnea Syndrome (OSAS) is a common sleep-related breathing disorder. Untreated OSAS leads to significant health consequences, disturbed functioning in society, decreased efficiency in a workplace and increased risk of accidents at work and while driving. The main patomechanisms of OSAS development are hypoxia, oxidative stress and inflammatory process. Intermittent hypoxia in OSAS patients is associated with subsequent episodes of reoxygenation with simultaneous increase of reactive oxygen species and reactive nitrogen species that stimulate secretion of extracellular metalloproteinases (MMPs). These compounds belong to a group of endogenous proteolytic enzymes produced by structural cells of extracellular matrix (ECM) and by cells of inflammatory response as well. ECMs are made of collagen proteins and glycoproteins. They form a scaffold for tissues of the soft palate. MMPs break down collagen molecules, which results in flaccidity of tissues, including tissues of the soft palate. The results of scientific studies have shown that expression, secretion, and activeness of MMPs increase during hypoxia. Thus metalloproteinases may be involved in the process of upper airway tissue damage during the intermittent hypoxia in OSAS.
金属蛋白酶在阻塞性睡眠呼吸暂停综合征发病机制中的作用
阻塞性睡眠呼吸暂停综合征(OSAS)是一种常见的与睡眠有关的呼吸障碍。未经治疗的OSAS会导致严重的健康后果,扰乱社会功能,降低工作场所的效率,增加工作和驾驶时发生事故的风险。缺氧、氧化应激和炎症过程是OSAS发生的主要病理机制。OSAS患者的间歇性缺氧与随后的再氧发作相关,同时增加活性氧和活性氮,刺激细胞外金属蛋白酶(MMPs)的分泌。这些化合物属于一组内源性蛋白水解酶,由细胞外基质结构细胞和炎症反应细胞产生。ecm由胶原蛋白和糖蛋白组成。它们形成软腭组织的支架。MMPs会分解胶原蛋白分子,导致组织松弛,包括软腭组织。科学研究结果表明,缺氧时MMPs的表达、分泌和活性增加。因此,金属蛋白酶可能参与了OSAS患者间歇性缺氧时上气道组织损伤的过程。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Polish Otorhinolaryngology Review
Polish Otorhinolaryngology Review Medicine-Otorhinolaryngology
CiteScore
0.20
自引率
0.00%
发文量
23
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