内皮功能障碍
氧化应激
血管紧张素II
一氧化氮
平衡
激素
内皮
线粒体
内分泌学
肾素-血管紧张素系统
内科学
活性氧
生物
医学
血压
细胞生物学
作者
Amir Ajoolabady,Domenico Praticò,Jun Ren
标识
DOI:10.1016/j.mce.2024.112309
摘要
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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