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细胞坏死性凋亡在发育中的大脑中的作用:神经发育障碍。

Necroptosis in the developing brain: role in neurodevelopmental disorders.

机构信息

The Neuro- Lab, School of Basic Medical Sciences, Federal University of Technology Akure, Akure, Nigeria.

Department of Human Anatomy, School of Basic Medical Sciences, Federal University of Technology Akure, Akure, Nigeria.

出版信息

Metab Brain Dis. 2023 Mar;38(3):831-837. doi: 10.1007/s11011-023-01203-9. Epub 2023 Mar 25.

DOI:10.1007/s11011-023-01203-9
PMID:36964816
Abstract

Cell death is vital to various organismal developmental processes including brain development. Apoptosis, the most recognized programmed cell death, has been linked to several developmental processes and implicated in pruning cells to provide the ultimate tissue integrity. However, more recently, other forms of non-apoptotic programmed cell death have been identified, of which necroptosis is of predominant interest. Necroptosis is a regulated form of necrosis, activated under apoptotic-deficient conditions. Tumour necrosis factor (TNF) is a major activator of necroptosis, and the process is mediated by several kinases including receptor-interacting protein kinase (RIPK) and mixed lineage kinase domain-like protein (MLKL). Potential roles for necroptosis during brain development have been muted. Necroptosis has been implicated in mediating neurological disorders, and contributing to the severity of these disorders. Here we will review the literature on the role of necroptosis in neurodevelopment, summarizing its molecular mechanisms and highlighting potential implications for disorders of the developing brain.

摘要

细胞死亡对于包括大脑发育在内的各种生物体发育过程至关重要。细胞凋亡是最被认可的程序性细胞死亡,与许多发育过程有关,并涉及到细胞的修剪,以提供最终的组织完整性。然而,最近,已经确定了其他形式的非凋亡程序性细胞死亡,其中坏死性细胞凋亡是主要关注的形式。坏死性细胞凋亡是一种受调控的坏死形式,在凋亡缺陷的情况下被激活。肿瘤坏死因子 (TNF) 是坏死性细胞凋亡的主要激活剂,该过程由几种激酶介导,包括受体相互作用蛋白激酶 (RIPK) 和混合谱系激酶结构域样蛋白 (MLKL)。坏死性细胞凋亡在大脑发育过程中的潜在作用受到抑制。坏死性细胞凋亡被认为在介导神经紊乱方面发挥作用,并导致这些紊乱的严重程度增加。在这里,我们将回顾关于坏死性细胞凋亡在神经发育中的作用的文献,总结其分子机制,并强调其对发育中大脑紊乱的潜在影响。

相似文献

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Necroptosis in the developing brain: role in neurodevelopmental disorders.细胞坏死性凋亡在发育中的大脑中的作用:神经发育障碍。
Metab Brain Dis. 2023 Mar;38(3):831-837. doi: 10.1007/s11011-023-01203-9. Epub 2023 Mar 25.
2
Tools in the Art of Studying Necroptosis.研究坏死性凋亡的方法
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The molecular mechanisms of MLKL-dependent and MLKL-independent necrosis.依赖 MLKL 和不依赖 MLKL 的细胞坏死的分子机制。
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PI3K mediates tumor necrosis factor induced-necroptosis through initiating RIP1-RIP3-MLKL signaling pathway activation.PI3K 通过启动 RIP1-RIP3-MLKL 信号通路激活介导肿瘤坏死因子诱导的细胞坏死。
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Receptor-interacting protein 3-phosphorylated Ca /calmodulin-dependent protein kinase II and mixed lineage kinase domain-like protein mediate intracerebral hemorrhage-induced neuronal necroptosis.受体相互作用蛋白3磷酸化的钙/钙调蛋白依赖性蛋白激酶II和混合谱系激酶结构域样蛋白介导脑出血诱导的神经元坏死性凋亡。
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The NS1 Protein of Influenza A Virus Participates in Necroptosis by Interacting with MLKL and Increasing Its Oligomerization and Membrane Translocation.甲型流感病毒 NS1 蛋白通过与 MLKL 相互作用并增加其寡聚化和膜转位来参与坏死性凋亡。
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Plasma membrane translocation of trimerized MLKL protein is required for TNF-induced necroptosis.三聚化 MLKL 蛋白向质膜易位是 TNF 诱导的坏死性凋亡所必需的。
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本文引用的文献

1
Necroptosis increases with age in the brain and contributes to age-related neuroinflammation.细胞程序性坏死随年龄增长在大脑中增加,并导致与年龄相关的神经炎症。
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HIST3H2A promotes the progression of prostate cancer through inhibiting cell necroptosis.HIST3H2A 通过抑制细胞坏死性凋亡促进前列腺癌的进展。
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The Fragile X Mental Retardation Protein Regulates RIPK1 and Colorectal Cancer Resistance to Necroptosis.脆性 X 智力低下蛋白调节 RIPK1 及结直肠癌对坏死性凋亡的抵抗作用。
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The potential role of necroptosis in inflammaging and aging.细胞坏死性凋亡在炎症衰老和衰老中的潜在作用。
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