Department of Drug Discovery and Development, Harrison College of Pharmacy, Auburn University, Auburn-AL 36849, USA.
Department of Cardiology, Zhongshan Hospital Fudan University, Shanghai 200032, China.
Acta Biochim Biophys Sin (Shanghai). 2023 Jun 25;55(8):1153-1167. doi: 10.3724/abbs.2023085.
Severe acute respiratory syndrome (SARS)-CoV-2 virus causes novel coronavirus disease 2019 (COVID-19), and there is a possible role for oxidative stress in the pathophysiology of neurological diseases associated with COVID-19. Excessive oxidative stress could be responsible for the thrombosis and other neuronal dysfunctions observed in COVID-19. This review discusses the role of oxidative stress associated with SARS-CoV-2 and the mechanisms involved. Furthermore, the various therapeutics implicated in treating COVID-19 and the oxidative stress that contributes to the etiology and pathogenesis of COVID-19-induced neuronal dysfunction are discussed. Further mechanistic and clinical research to combat COVID-19 is warranted to understand the exact mechanisms, and its true clinical effects need to be investigated to minimize neurological complications from COVID-19.
严重急性呼吸系统综合症(SARS)-冠状病毒 2 型(SARS-CoV-2)引发 2019 年新型冠状病毒疾病(COVID-19),氧化应激可能在与 COVID-19 相关的神经疾病的病理生理学中发挥作用。过多的氧化应激可能是导致 COVID-19 中观察到的血栓和其他神经元功能障碍的原因。本综述讨论了与 SARS-CoV-2 相关的氧化应激及其涉及的机制。此外,还讨论了治疗 COVID-19 中涉及的各种治疗方法以及导致 COVID-19 引起的神经元功能障碍的发病机制的氧化应激。为了理解确切的机制并最大程度地减少 COVID-19 引起的神经并发症,需要进行进一步的机制和临床研究来对抗 COVID-19。