Angiotensin II: Role in oxidative stress, endothelial dysfunction, and diseases

被引:2
|
作者
Ajoolabady, Amir [1 ]
Pratico, Domenico [2 ]
Ren, Jun [3 ,4 ]
机构
[1] Univ Alabama Birmingham, Dept Biomed Engn, Birmingham, AL 35294 USA
[2] Temple Univ, Alzheimers Ctr Temple, Lewis Katz Sch Med, Philadelphia, PA 19140 USA
[3] Fudan Univ, Zhongshan Hosp, Shanghai Inst Cardiovasc Dis, Dept Cardiol, Shanghai 200032, Peoples R China
[4] Natl Clin Res Ctr Intervent Med, Shanghai 200032, Peoples R China
基金
中国国家自然科学基金;
关键词
Angiotensin II; Oxidative stress; Mitochondrial damage; Vascular diseases; NITRIC-OXIDE; INHIBITION; SUPEROXIDE; MECHANISMS;
D O I
10.1016/j.mce.2024.112309
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
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 IImediated 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.
引用
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页数:5
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