Al-Kuraishy Hayder M, Al-Hamash Sadiq M, Jabir Majid S, Al-Gareeb Ali I, Albuhadily Ali K, Albukhaty Salim, Sulaiman Ghassan M
Department of Clinical pharmacology and Medicine, College of Medicine, Mustansiriyah University, Baghdad, Iraq.
Department of Pediatric Cardiology, College of Medicine, Mustansiriyah University, Baghdad, Iraq.
Ageing Res Rev. 2024 Feb;94:102200. doi: 10.1016/j.arr.2024.102200. Epub 2024 Jan 17.
Parkinson disease (PD) is a common brain neurodegenerative disease due to progressive degeneration of the dopaminergic neurons in the substantia nigra pars compacta (SNpc). Of note, the cardio-metabolic disorders such as hypertension are adversely affect PD neuropathology through exaggeration of renin-angiotensin system (RAS). The RAS affects the stability of dopaminergic neurons in the SNpc, and exaggeration of angiotensin II (AngII) is implicated in the development and progression of PD. RAS has two axes classical including angiotensin converting enzyme (ACE)/AngII/AT1R, and the non-classical axis which include ACE2/Ang1-7/Mas receptor, AngIII, AngIV, AT2R, and AT4R. It has been shown that brain RAS is differs from that of systemic RAS that produce specific neuronal effects. As well, there is an association between brain RAS and PD. Therefore, this review aims to revise from published articles the role of brain RAS in the pathogenesis of PD focusing on the non-classical pathway, and how targeting of this axis can modulate PD neuropathology.
帕金森病（PD）是一种常见的脑部神经退行性疾病，由黑质致密部（SNpc）中多巴胺能神经元的进行性退化引起。值得注意的是，高血压等心脏代谢紊乱会通过肾素-血管紧张素系统（RAS）的过度激活对PD神经病理学产生不利影响。RAS影响SNpc中多巴胺能神经元的稳定性，而血管紧张素II（AngII）的过度激活与PD的发生和发展有关。RAS有两个经典轴，包括血管紧张素转换酶（ACE）/AngII/AT1R，以及非经典轴，包括ACE2/Ang1-7/Mas受体、AngIII、AngIV、AT2R和AT4R。研究表明，脑RAS与产生特定神经元效应的全身RAS不同。此外，脑RAS与PD之间存在关联。因此，本综述旨在从已发表的文章中修订脑RAS在PD发病机制中的作用，重点关注非经典途径，以及靶向该轴如何调节PD神经病理学。
