氧化应激在损伤和高血压中的作用
Willaim J Arendshorst1, Aleksandr E Vendrov2, Nitin Kumar2,3
1Department of Cell Biology and Physiology, University of North Carolina, Chapel Hill, NC 27599, USA.
Antioxidants (Basel, Switzerland)
|January 8, 2025
概括
高血压会损害脏,增加中风和心脏病的风险. 通过向氧化应激,炎症和氨酸- ангиотензин- 阿尔多斯特系统 (RAAS) 来控制血压是预防损伤和疾病进展的关键.
科学领域:
- 腎臟病學 (nephrology) 是一種醫學專業.
- 心血管医学 心血管医学
- 遗传学 遗传学 是一个
背景情况:
- 高血压 (HTN) 是损伤的主要驱动因素,包括硬化和高血压病,导致慢性病 (CKD) 和末期病 (ESRD).
- 此外,HTN还会增加中风和冠心病的风险.
- 氧化应激,炎症和氨酸- ангиотензин- 阿尔多素系统 (RAAS) 激活是HTN诱导损伤的关键调解者.
研究的目的:
- 审查NADPH氧化酶 (NOX) 在高血压相关损伤中的作用.
- 通过准关键的病理生理路径,突出管理血压 (BP) 的重要性.
- 讨论遗传和环境因素对高血压损伤的影响.
主要方法:
- 审查有关高血压,病,氧化应激和RAAS的现有文献.
- 对动物模型 (如自发高血压大鼠) 的分析,以了解HTN的病原性.
- 检查反应性氧物种 (ROS) 和NOX异构体在血压调节和功能中的作用.
主要成果:
- 过度生产ROS,特别是通过NOX酶,显著促进HTN的发展和进展,损害功能.
- 遗传和环境因素,包括肠道微生物组的改变,影响对高血压损伤的易感性.
- 向NOX以减少ROS,以及RAAS抑制,抗炎和抗氧化策略,显示出对脏和抗高血压保护的承诺.
结论:
- 在HTN及其并发症的发病和进展中,NOX起着关键作用.
- 有效的血压管理需要解决氧化应激,炎症和RAAS激活.
- 新兴的疗法,如SGLT2抑制剂和矿物质皮质体受体对抗剂,通过减轻这些途径,在管理HTN和CKD方面提供潜在的好处.
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