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本文引用的文献

1
Cleavage Region Thyrotropin Receptor Antibodies Influence Thyroid Cell Survival .解育区促甲状腺激素受体抗体影响甲状腺细胞的存活。
Thyroid. 2019 Jul;29(7):993-1002. doi: 10.1089/thy.2018.0633. Epub 2019 Jun 4.
2
Stimulatory TSH-Receptor Antibodies and Oxidative Stress in Graves Disease.刺激型促甲状腺素受体抗体与格雷夫斯病的氧化应激。
J Clin Endocrinol Metab. 2018 Oct 1;103(10):3668-3677. doi: 10.1210/jc.2018-00509.
3
Biased signaling by thyroid-stimulating hormone receptor-specific antibodies determines thyrocyte survival in autoimmunity.甲状腺刺激素受体特异性抗体的信号偏向决定了自身免疫中甲状腺细胞的存活。
Sci Signal. 2018 Jan 23;11(514):eaah4120. doi: 10.1126/scisignal.aah4120.
4
Epac2-Rap1 Signaling Regulates Reactive Oxygen Species Production and Susceptibility to Cardiac Arrhythmias.Epac2-Rap1信号通路调控活性氧生成及对心律失常的易感性。
Antioxid Redox Signal. 2017 Jul 20;27(3):117-132. doi: 10.1089/ars.2015.6485. Epub 2016 Oct 27.
5
Constitutive activities in the thyrotropin receptor: regulation and significance.促甲状腺激素受体的组成性活性:调节与意义
Adv Pharmacol. 2014;70:81-119. doi: 10.1016/B978-0-12-417197-8.00003-1.
6
How one TSH receptor antibody induces thyrocyte proliferation while another induces apoptosis.一种促甲状腺激素受体抗体如何诱导甲状腺细胞增殖,而另一种却诱导其凋亡。
J Autoimmun. 2013 Dec;47:17-24. doi: 10.1016/j.jaut.2013.07.009. Epub 2013 Aug 17.
7
NADPH oxidase NOX2 defines a new antagonistic role for reactive oxygen species and cAMP/PKA in the regulation of insulin secretion.NADPH 氧化酶 NOX2 定义了活性氧和 cAMP/PKA 在胰岛素分泌调节中的新拮抗作用。
Diabetes. 2012 Nov;61(11):2842-50. doi: 10.2337/db12-0009. Epub 2012 Aug 28.
8
The unfolded protein response: controlling cell fate decisions under ER stress and beyond.未折叠蛋白反应:在 ER 应激及其他情况下控制细胞命运决定。
Nat Rev Mol Cell Biol. 2012 Jan 18;13(2):89-102. doi: 10.1038/nrm3270.
9
The role of oxidative stress on the pathogenesis of graves' disease.氧化应激在格雷夫斯病发病机制中的作用。
J Thyroid Res. 2012;2012:302537. doi: 10.1155/2012/302537. Epub 2011 Dec 10.
10
Mitochondria-ros crosstalk in the control of cell death and aging.线粒体-活性氧在细胞死亡和衰老调控中的相互作用
J Signal Transduct. 2012;2012:329635. doi: 10.1155/2012/329635. Epub 2011 Nov 14.

了解甲状腺细胞应激。

Understanding Thyroid Cell Stress.

机构信息

Thyroid Research Unit, Icahn School of Medicine at Mount Sinai, and the James J. Peters VA Medical Center, New York, New York.

出版信息

J Clin Endocrinol Metab. 2020 Mar 1;105(3):e66-9. doi: 10.1210/clinem/dgz193.

DOI:10.1210/clinem/dgz193
PMID:31711166
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7047584/
Abstract

Understanding the regulatory mechanisms that control intracellular stress has fundamental importance since its failure results in cell death. Evidence has emerged indicating that the intracellular signals that are induced in response to diverse stresses include the deoxyribonucleic acid damage response, the unfolded protein response, the mitochondrial and/or endoplasmic reticulum stress responses, and the autophagy signals to degrade dangerous protein aggregates. These signals bring changes to the stressed cells that may support systemic homeostasis or contribute to disease pathology. In normal thyroid cells, both reactive oxygen species (ROS) and antioxidant (AOD) activity is low. An increase in ROS balanced by AOD leads only to mild inflammation, but unopposed increases in ROS lead to a strong inflammatory response and may result in apoptosis. A balance between ROS and AOD is, therefore, needed to maintain thyrocyte homeostasis. This perspective describes how thyroid cells are subjected to multiple insults and how they try to protect themselves using these different cellular responses.

摘要

理解控制细胞内应激的调节机制至关重要,因为其失败会导致细胞死亡。有证据表明,细胞对各种应激的反应包括脱氧核糖核酸损伤反应、未折叠蛋白反应、线粒体和/或内质网应激反应以及自噬信号以降解危险的蛋白质聚集体。这些信号会给应激细胞带来变化,这些变化可能有助于维持全身的内稳态,也可能导致疾病的病理变化。在正常甲状腺细胞中,活性氧(ROS)和抗氧化(AOD)的活性都很低。ROS 的增加被 AOD 平衡只会导致轻度炎症,但 ROS 的无拮抗增加会导致强烈的炎症反应,并可能导致细胞凋亡。因此,需要在 ROS 和 AOD 之间取得平衡,以维持甲状腺细胞的内稳态。本文从多个方面描述了甲状腺细胞如何受到多种损伤,以及它们如何利用这些不同的细胞反应来保护自己。