Implications of Iron in Ferroptosis, Necroptosis, and Pyroptosis as Potential Players in TBI Morbidity and Mortality.

IF 3.9 4区 医学 Q2 NEUROSCIENCES ASN NEURO Pub Date : 2024-01-01 Epub Date: 2024-09-09 DOI:10.1080/17590914.2024.2394352
Makenzie Nolt, James Connor
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引用次数: 0

Abstract

Iron is a critical transition metal required to sustain a healthy central nervous system. Iron is involved in metabolic reactions, enzymatic activity, myelinogenesis, and oxygen transport. However, in several pathological conditions such as cancer, neurodegeneration, and neurotrauma iron becomes elevated. Excessive iron can have deleterious effects leading to reactive oxygen species (ROS) via the Fenton reaction. Iron-derived ROS are known to drive several mechanisms such as cell death pathways including ferroptosis, necroptosis, and pyroptosis. Excessive iron present in the post-traumatic brain could trigger these harmful pathways potentiating the high rates of morbidity and mortality. In the present review, we will discuss how iron plays an intricate role in initiating ferroptosis, necroptosis, and pyroptosis, examine their potential link to traumatic brain injury morbidity and mortality, and suggest therapeutic targets.

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铁败血病、坏死病和热败血病中的铁作为创伤性脑损伤发病率和死亡率的潜在参与者的影响。
铁是维持中枢神经系统健康所需的重要过渡金属。铁参与新陈代谢反应、酶活性、髓鞘生成和氧运输。然而,在癌症、神经变性和神经创伤等几种病理情况下,铁会升高。过量的铁会产生有害影响,通过芬顿反应产生活性氧(ROS)。已知铁衍生的 ROS 可驱动多种机制,如细胞死亡途径,包括铁凋亡、坏死和热凋亡。创伤后大脑中过量的铁可能会触发这些有害途径,从而加剧高发病率和死亡率。在本综述中,我们将讨论铁如何在启动铁变态反应、坏死和热变态反应中发挥复杂的作用,研究它们与创伤性脑损伤发病率和死亡率的潜在联系,并提出治疗目标。
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来源期刊
ASN NEURO
ASN NEURO NEUROSCIENCES-
CiteScore
7.70
自引率
4.30%
发文量
35
审稿时长
>12 weeks
期刊介绍: ASN NEURO is an open access, peer-reviewed journal uniquely positioned to provide investigators with the most recent advances across the breadth of the cellular and molecular neurosciences. The official journal of the American Society for Neurochemistry, ASN NEURO is dedicated to the promotion, support, and facilitation of communication among cellular and molecular neuroscientists of all specializations.
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