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铁死亡调控缺血性脑卒中的机制及其在缺血性脑卒中治疗中抑制铁死亡的药理学作用。

Mechanism of ferroptosis regulating ischemic stroke and pharmacologically inhibiting ferroptosis in treatment of ischemic stroke.

机构信息

Department of Neurosurgery, First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou City, China.

出版信息

CNS Neurosci Ther. 2024 Jul;30(7):e14865. doi: 10.1111/cns.14865.

Abstract

Ferroptosis is a newly discovered form of programmed cell death that is non-caspase-dependent and is characterized by the production of lethal levels of iron-dependent lipid reactive oxygen species (ROS). In recent years, ferroptosis has attracted great interest in the field of cerebral infarction because it differs morphologically, physiologically, and genetically from other forms of cell death such as necrosis, apoptosis, autophagy, and pyroptosis. In addition, ROS is considered to be an important prognostic factor for ischemic stroke, making it a promising target for stroke treatment. This paper summarizes the induction and defense mechanisms associated with ferroptosis, and explores potential treatment strategies for ischemic stroke in order to lay the groundwork for the development of new neuroprotective drugs.

摘要

铁死亡是一种新发现的程序性细胞死亡形式,其特征为铁依赖性脂质活性氧(ROS)的产生达到致死水平,但不依赖于胱天蛋白酶。近年来,铁死亡因其在形态、生理和遗传上与细胞坏死、细胞凋亡、自噬和细胞焦亡等其他形式的细胞死亡不同,而在脑梗死领域引起了广泛关注。此外,ROS 被认为是缺血性脑卒中的一个重要预后因素,因此它成为了治疗脑卒中的一个有前景的靶点。本文总结了与铁死亡相关的诱导和防御机制,并探讨了缺血性脑卒中的潜在治疗策略,以期为新型神经保护药物的开发奠定基础。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/79f5/11265528/7e94ba685434/CNS-30-e14865-g003.jpg

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