Department of Forensic Medicine, School of Basic Medicine and Biological Sciences, Soochow University, Suzhou 215123, China.
School of Forensic Medicine, Wannan Medical College, Wuhu 241002, China.
Oxid Med Cell Longev. 2022 Jul 22;2022:3999083. doi: 10.1155/2022/3999083. eCollection 2022.
With the acceleration of population aging, nervous system diseases including Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD), anxiety, depression, stroke, and traumatic brain injury (TBI) have become a huge burden on families and society. The mechanism of neurological disorders is complex, which also lacks effective treatment, so relevant research is required to solve these problems urgently. Given that oxidative stress-induced lipid peroxidation eventually leads to ferroptosis, both oxidative stress and ferroptosis are important mechanisms causing neurological disorders, targeting mediators of oxidative stress and ferroptosis have become a hot research direction at present. Our review provides a current view of the mechanisms underlying ferroptosis and oxidative stress participate in neurological disorders, the potential application of molecular mediators targeting ferroptosis and oxidative stress in neurological disorders. The target of molecular mediators or agents of oxidative stress and ferroptosis associated with neurological disorders, such as reactive oxygen species (ROS), nuclear factor erythroid 2-related factor-antioxidant response element (Nrf2-ARE), n-acetylcysteine (NAC), Fe, NADPH, and its oxidases NOX, has been described in this article. Given that oxidative stress-induced ferroptosis plays a pivotal role in neurological disorders, further research on the mechanisms of ferroptosis caused by oxidative stress will help provide new targets for the treatment of neurological disorders.
随着人口老龄化的加速,包括阿尔茨海默病(AD)、帕金森病(PD)、亨廷顿病(HD)、焦虑、抑郁、中风和创伤性脑损伤(TBI)在内的神经系统疾病已成为家庭和社会的巨大负担。神经系统疾病的发病机制复杂,且缺乏有效的治疗手段,因此需要相关研究来迫切解决这些问题。鉴于氧化应激诱导的脂质过氧化最终导致铁死亡,氧化应激和铁死亡都是导致神经系统疾病的重要机制,针对氧化应激和铁死亡的介质已成为当前的热门研究方向。我们的综述提供了铁死亡和氧化应激参与神经系统疾病的机制的最新观点,以及针对铁死亡和氧化应激的分子介质在神经系统疾病中的潜在应用。本文描述了与神经系统疾病相关的氧化应激和铁死亡的分子介质或剂的靶点,如活性氧(ROS)、核因子红细胞 2 相关因子-抗氧化反应元件(Nrf2-ARE)、N-乙酰半胱氨酸(NAC)、Fe、NADPH 及其氧化酶 NOX。鉴于氧化应激诱导的铁死亡在神经系统疾病中起着关键作用,对氧化应激引起的铁死亡机制的进一步研究将有助于为神经系统疾病的治疗提供新的靶点。