血管紧张素 II:在氧化应激、内皮功能障碍和疾病中的作用

IF 3.8 3区 医学 Q2 CELL BIOLOGY Molecular and Cellular Endocrinology Pub Date : 2024-06-08 DOI:10.1016/j.mce.2024.112309
Amir Ajoolabady , Domenico Pratico , Jun Ren
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引用次数: 0

摘要

血管紧张素 II(Ang II)是一种蛋白质激素,能够通过多种机制对血压进行生理调节。血管紧张素 II 主要由肝脏产生,处于平衡状态。然而,Ang II 的过量产生与体内一系列病理事件密切相关。内皮功能障碍就是其中一种可导致血管异常的病理事件。内皮细胞(ECs)过度暴露于 Ang II 可通过多种机制诱发内皮功能障碍。其中一种机制是 Ang II 介导的线粒体氧化应激。在这篇微型综述中,我们旨在讨论 Ang II 通过线粒体氧化应激介导的内皮功能障碍的分子机制以及一氧化氮在 EC 中的保护作用。破译这些机制可能会发现新的治疗策略,以预防血液中 Ang II 浓度升高引起的内皮功能障碍和相关疾病。
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Angiotensin II: Role in oxidative stress, endothelial dysfunction, and diseases

Angiotensin II (Ang II) is a protein hormone capable of physiologically regulating blood pressure through diverse mechanisms. Ang II is mainly produced by the liver at homeostatic levels. However, excessive production of Ang II is closely associated with a series of pathological events in the body. The endothelial dysfunction is one of these pathological events that can drive vascular anomalies. The excessive exposure of endothelial cells (ECs) to Ang II may induce endothelial dysfunction via diverse mechanisms. One of these mechanisms is Ang II-mediated mitochondrial oxidative stress. In this mini-review, we aimed to discuss the molecular mechanisms of Ang II-mediated endothelial dysfunction through mitochondrial oxidative stress and the protective role of nitric oxide in ECs. Deciphering these mechanisms may disclose novel therapeutic strategies to prevent endothelial dysfunction and associated diseases induced by elevated leves of Ang II in the blood.

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来源期刊
Molecular and Cellular Endocrinology
Molecular and Cellular Endocrinology 医学-内分泌学与代谢
CiteScore
9.00
自引率
2.40%
发文量
174
审稿时长
42 days
期刊介绍: Molecular and Cellular Endocrinology was established in 1974 to meet the demand for integrated publication on all aspects related to the genetic and biochemical effects, synthesis and secretions of extracellular signals (hormones, neurotransmitters, etc.) and to the understanding of cellular regulatory mechanisms involved in hormonal control.
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