慢性间歇性缺氧引起的心血管和功能障碍:从适应到不适应
Claire Arnaud1, Emma Billoir1, Antonio F de Melo Junior2
1Université Grenoble-Alpes INSERM U1300, Laboratoire HP2, Grenoble, France.
The Journal of physiology
|October 26, 2023
概括
慢性间歇性缺氧 (CIH),常见于阻塞性睡眠呼吸暂停 (OSA),驱动高血压和心脏病. 研究突出了分子途径和针对已确定的疾病的向治疗的需要.
科学领域:
- 心血管和脏医学 心血管和脏医学
- 睡眠医学 睡眠医学
- 分子病理学分子病理学
背景情况:
- 阻塞性睡眠呼吸暂停 (OSA) 很普遍,与心血管和脏疾病有关,主要是由于慢性间歇性缺氧 (CIH).
- CIH诱导的高血压涉及同情性过度活跃和持续的分子变化,但对于已确定的疾病的有效干预措施尚不清楚.
- CIH对血管和心脏组织产生负面影响,促进内皮功能障碍,动脉样硬化,心房动和心脏重塑.
研究的目的:
- 审查CIH诱导的高血压和心脏脏损伤背后的分子机制.
- 探索已确定的CIH相关高血压干预措施的有效性.
- 讨论针对间歇性缺氧而产生的心结局的异质性,以及对表型分层的需要.
主要方法:
- 对CIH诱导的高血压,血管功能障碍,心脏损伤和病中的分子机制的文献综述.
- 分析促炎,促氧化和信号通路 (例如,氧化,HIF-1α,TLR4/NF-κB/NLRP3炎症体).
- 检查新出现的治疗点,包括肠-轴和亚利碳化合物受体 (AhR) 阻塞.
主要成果:
- CIH通过交感过度活动和分子途径驱动高血压,导致内皮功能障碍,血管重塑和加速动脉样硬化.
- 心肌的影响包括心房动,心脏重塑和收缩功能障碍,由氧化应激,炎症和信号干扰驱动.
- 损伤涉及TLR4/NF-κB/NLRP3炎症酶激活和热,导致高血压和慢性病.
结论:
- 通过复杂的分子通路,CIH深深地影响心血管和系统,需要对治疗干预措施有更深入的理解.
- 针对肠-轴和AhR的新兴疗法显示出减轻CIH相关损伤的希望.
- 基于心脏结结果对OSA表型的分层对开发有效的个性化治疗策略至关重要.
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