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本文引用的文献

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Acute Respiratory Distress Syndrome.急性呼吸窘迫综合征
JAMA. 2018 Feb 20;319(7):732. doi: 10.1001/jama.2018.0483.
2
Biological functions and role of mitogen-activated protein kinase activated protein kinase 2 (MK2) in inflammatory diseases.丝裂原活化蛋白激酶激活的蛋白激酶 2(MK2)在炎症性疾病中的生物学功能和作用。
Pharmacol Rep. 2017 Aug;69(4):746-756. doi: 10.1016/j.pharep.2017.03.023. Epub 2017 Apr 8.
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Evidence of Presynaptic Localization and Function of the c-Jun N-Terminal Kinase.c-Jun氨基末端激酶的突触前定位及功能证据
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4
Nur77 attenuates endothelin-1 expression via downregulation of NF-κB and p38 MAPK in A549 cells and in an ARDS rat model.在A549细胞和急性呼吸窘迫综合征(ARDS)大鼠模型中,Nur77通过下调核因子κB(NF-κB)和p38丝裂原活化蛋白激酶(p38 MAPK)来减弱内皮素-1的表达。
Am J Physiol Lung Cell Mol Physiol. 2016 Dec 1;311(6):L1023-L1035. doi: 10.1152/ajplung.00043.2016. Epub 2016 Oct 7.
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Brain-Derived Neurotrophic Factor Inhibits Intercellular Adhesion Molecule-1 Expression in Interleukin-1β-Treated Endothelial Cells.脑源性神经营养因子抑制白细胞介素-1β处理的内皮细胞中细胞间黏附分子-1的表达。
Cell Biochem Biophys. 2016 Sep;74(3):399-406. doi: 10.1007/s12013-016-0749-2. Epub 2016 Jun 17.
6
The MK2/HuR signaling pathway regulates TNF-α-induced ICAM-1 expression by promoting the stabilization of ICAM-1 mRNA.MK2/HuR信号通路通过促进细胞间黏附分子-1(ICAM-1)mRNA的稳定性来调节肿瘤坏死因子-α(TNF-α)诱导的ICAM-1表达。
BMC Pulm Med. 2016 May 23;16(1):84. doi: 10.1186/s12890-016-0247-8.
7
HMGB1 Mediates Anemia of Inflammation in Murine Sepsis Survivors.高迁移率族蛋白B1介导小鼠脓毒症幸存者的炎症性贫血。
Mol Med. 2016 May;21(1):951-958. doi: 10.2119/molmed.2015.00243. Epub 2015 Dec 29.
8
Preconditioning of physiological cyclic stretch attenuated HMGB1 expression in pathologically mechanical stretch-activated A549 cells and ventilator-induced lung injury rats through inhibition of IL-6/STAT3/SOCS3.生理性周期性拉伸预处理通过抑制IL-6/STAT3/SOCS3减轻了病理性机械拉伸激活的A549细胞和呼吸机诱导的肺损伤大鼠中HMGB1的表达。
Int Immunopharmacol. 2016 Feb;31:66-73. doi: 10.1016/j.intimp.2015.12.017. Epub 2015 Dec 17.
9
Role of pulmonary microvascular endothelial cell apoptosis in murine sepsis-induced lung injury in vivo.肺微血管内皮细胞凋亡在小鼠体内脓毒症诱导的肺损伤中的作用
Respir Res. 2015 Sep 16;16(1):109. doi: 10.1186/s12931-015-0266-7.
10
Mouse Models of Acute Respiratory Distress Syndrome: A Review of Analytical Approaches, Pathologic Features, and Common Measurements.急性呼吸窘迫综合征的小鼠模型:分析方法、病理特征及常用测量指标综述
Toxicol Pathol. 2015 Dec;43(8):1074-92. doi: 10.1177/0192623315598399. Epub 2015 Aug 21.

p38MAPK 在急性呼吸窘迫综合征的发展中起着关键作用。

p38MAPK plays a pivotal role in the development of acute respiratory distress syndrome.

机构信息

Department of Intensive Care Unit, Taihe Hospital, Hubei University of Medicine, Shiyan 442000, Hubei Province, China.

Institute of Biomedical Research, Taihe Hospital, Hubei University of Medicine, Shiyan 442000, Hubei Province, China.

出版信息

Clinics (Sao Paulo). 2019;74:e509. doi: 10.6061/clinics/2019/e509. Epub 2019 Aug 12.

DOI:10.6061/clinics/2019/e509
PMID:31411275
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6683303/
Abstract

Acute respiratory distress syndrome (ARDS) is a life-threatening illness characterized by a complex pathophysiology, involving not only the respiratory system but also nonpulmonary distal organs. Although advances in the management of ARDS have led to a distinct improvement in ARDS-related mortality, ARDS is still a life-threatening respiratory condition with long-term consequences. A better understanding of the pathophysiology of this condition will allow us to create a personalized treatment strategy for improving clinical outcomes. In this article, we present a general overview p38 mitogen-activated protein kinase (p38MAPK) and recent advances in understanding its functions. We consider the potential of the pharmacological targeting of p38MAPK pathways to treat ARDS.

摘要

急性呼吸窘迫综合征(ARDS)是一种危及生命的疾病,其病理生理学十分复杂,不仅涉及呼吸系统,还涉及非肺部的远隔器官。尽管 ARDS 管理方面的进展显著改善了与 ARDS 相关的死亡率,但 ARDS 仍然是一种危及生命的呼吸系统疾病,会带来长期后果。更好地了解这种疾病的病理生理学将使我们能够制定个性化的治疗策略,以改善临床结局。本文概述了 p38 丝裂原活化蛋白激酶(p38MAPK)的一般情况及其功能的最新进展。我们考虑了针对 p38MAPK 途径进行药理学靶向治疗 ARDS 的潜力。