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本文引用的文献

1
Involvement of the unfolded protein response in the protective effects of growth hormone releasing hormone antagonists in the lungs.未折叠蛋白反应在生长激素释放激素拮抗剂对肺部的保护作用中的参与。
J Cell Commun Signal. 2021 Mar;15(1):125-129. doi: 10.1007/s12079-020-00593-0. Epub 2020 Nov 13.
2
Evaluating endoplasmic reticulum stress and unfolded protein response through the lens of ecology and evolution.从生态学和进化的角度评估内质网应激和未折叠蛋白反应。
Biol Rev Camb Philos Soc. 2021 Apr;96(2):541-556. doi: 10.1111/brv.12667. Epub 2020 Nov 8.
3
Growth Hormone-Releasing Hormone in Lung Physiology and Pulmonary Disease.生长激素释放激素在肺生理学和肺部疾病中的作用。
Cells. 2020 Oct 21;9(10):2331. doi: 10.3390/cells9102331.
4
Luminespib counteracts the Kifunensine-induced lung endothelial barrier dysfunction.鲁米斯匹布可对抗基夫内新诱导的肺内皮屏障功能障碍。
Curr Res Toxicol. 2020 Jun 10;1:111-115. doi: 10.1016/j.crtox.2020.09.003. Epub 2020 Sep 24.
5
P53 is Subjected to Lipoteichoic Acid-Induced Phosphorylation in the Lungs.p53在肺中受到脂磷壁酸诱导的磷酸化作用。
TH Open. 2020 Aug 20;4(3):e173-e174. doi: 10.1055/s-0040-1714695. eCollection 2020 Jul.
6
Kifunensine compromises lung endothelial barrier function.基伏那辛会损害肺内皮屏障功能。
Microvasc Res. 2020 Nov;132:104051. doi: 10.1016/j.mvr.2020.104051. Epub 2020 Jul 28.
7
Effects of Heat Shock Protein 90 Inhibition In the Lungs.热休克蛋白90抑制在肺部的作用
Med Drug Discov. 2020 Jun;6. doi: 10.1016/j.medidd.2020.100046. Epub 2020 May 17.
8
P53 deficiency potentiates LPS-Induced acute lung injury .P53基因缺陷会加重脂多糖诱导的急性肺损伤。
Curr Res Physiol. 2020 Dec;3:30-33. doi: 10.1016/j.crphys.2020.07.001. Epub 2020 Jul 9.
9
Heat shock protein 90 inhibition in the inflamed lungs.在炎症肺部中抑制热休克蛋白 90。
Cell Stress Chaperones. 2020 Mar;25(2):195-197. doi: 10.1007/s12192-020-01069-1. Epub 2020 Jan 17.
10
Hsp90 inhibitors induce the unfolded protein response in bovine and mice lung cells.Hsp90 抑制剂诱导牛和小鼠肺细胞发生未折叠蛋白反应。
Cell Signal. 2020 Mar;67:109500. doi: 10.1016/j.cellsig.2019.109500. Epub 2019 Dec 16.

未折叠蛋白反应:内皮屏障的一种调节因子。

Unfolded Protein Response: A Regulator of the Endothelial Barrier.

作者信息

Barabutis Nektarios

机构信息

School of Basic Pharmaceutical and Toxicological Sciences, College of Pharmacy, University of Louisiana Monroe, Monroe, Louisiana 71201, USA.

出版信息

Endocr Metab Sci. 2021 Jun 30;3. doi: 10.1016/j.endmts.2021.100092. Epub 2021 Mar 4.

DOI:10.1016/j.endmts.2021.100092
PMID:33796874
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8009497/
Abstract

Recent evidence suggest that the endothelial barrier function is enhanced by the mild activation of the unfolded protein response (UPR), which aims to suppress abnormal increases of endoplasmic reticulum stress. Heat shock protein 90 inhibitors and growth hormone releasing hormone antagonists exert the capacity to activate this multifaceted cellular mechanism (UPR). Thus, investigations on the signalling network involved in those events, may deliver exciting opportunities in diseases related to endothelial barrier dysfunction. The diverse spectrum of those pathologies include sepsis and Acute Respiratory Distress Syndrome (ARDS).

摘要

最近的证据表明,未折叠蛋白反应(UPR)的轻度激活可增强内皮屏障功能,该反应旨在抑制内质网应激的异常增加。热休克蛋白90抑制剂和生长激素释放激素拮抗剂具有激活这种多方面细胞机制(UPR)的能力。因此,对参与这些事件的信号网络进行研究,可能会为与内皮屏障功能障碍相关的疾病带来令人兴奋的机遇。这些病理状况的范围广泛,包括败血症和急性呼吸窘迫综合征(ARDS)。