当化应激袭击内质网膜时:可能对oxLDL/oxysterols诱导的内皮功能障碍产生影响
M G Nasoni1, R Crinelli1, L Iuliano2
1Department of Biomolecular Sciences, University of Urbino Carlo Bo, Urbino, Italy.
Free radical biology & medicine
|August 6, 2023
概括
氧化LDL和氧醇通过内细胞网膜压力导致内皮功能障碍. 本综述探讨了氧化的过度生产和化压力如何与这种压力有关,影响内皮细胞.
科学领域:
- 心血管生物学 心血管生物学
- 内皮细胞生物学 内皮细胞生物学
- 分子医学是分子医学.
背景情况:
- 氧化低密度脂蛋白 (oxLDL) 和氧醇是导致内皮功能障碍 (ED) 的关键因素.
- 细胞内膜网膜应激 (ERS),炎症和亡是由oxLDL和oxysterols诱导的,但机制尚不清楚.
- 过度的氧化 (NO) 生产,反应性物种 (RNS),化应激 (NSS) 和蛋白质S-化都与病理有关.
研究的目的:
- 审查oxLDL/oxysterol诱导的ED中NO和ERS之间的关联.
- 阐明在内皮细胞中连接NSS和ERS的分子机制.
- 提出针对ED的治疗策略的框架.
主要方法:
- 对现有证据的文献审查.
- 对涉及NO,RNS,NSS和ERS的分子通路的分析.
- 专注于内皮细胞信号传递.
主要成果:
- 有证据将NO的过度生产和NSS与ERS联系起来.
- NSS和S-化可以扰乱ER信号通路.
- 乱的NO合成可能会影响内皮细胞中的信号效应器.
结论:
- 在oxLDL/oxysterol引起的ED的背景下,氧化在ERS中起着重要作用.
- 了解NSS和ERS之间的相互作用对于ED至关重要.
- 进一步的研究可以指导针对ED的新型治疗干预.
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