Impaired AMPK Activity Drives Age-Associated Acute Lung Injury after Hemorrhage.
作者信息
Southern Brian D, Scheraga Rachel G, Olman Mitchell A
机构信息
1 Cleveland Clinic Respiratory Institute Lerner Research Institute Department of Pathobiology Cleveland, Ohio.
出版信息
Am J Respir Cell Mol Biol. 2017 May;56(5):553-555. doi: 10.1165/rcmb.2017-0023ED.
Abstract
摘要
相似文献
1
Impaired AMPK Activity Drives Age-Associated Acute Lung Injury after Hemorrhage.AMPK活性受损促使出血后发生与年龄相关的急性肺损伤。
Am J Respir Cell Mol Biol. 2017 May;56(5):553-555. doi: 10.1165/rcmb.2017-0023ED.
2
IL-10 administration attenuates pulmonary neutrophil infiltration and alters pulmonary iNOS activation following hemorrhagic shock.给予白细胞介素-10可减轻失血性休克后肺内中性粒细胞浸润，并改变肺内诱导型一氧化氮合酶的激活状态。
Inflamm Res. 2009 Mar;58(3):170-4. doi: 10.1007/s00011-009-8116-z.
3
IL-10 deficiency augments acute lung but not liver injury in hemorrhagic shock.白细胞介素-10缺乏会加剧失血性休克中的急性肺损伤，但不会加剧肝损伤。
Cytokine. 2009 Jan;45(1):26-31. doi: 10.1016/j.cyto.2008.10.004. Epub 2008 Nov 17.
4
Osthol attenuates neutrophilic oxidative stress and hemorrhagic shock-induced lung injury via inhibition of phosphodiesterase 4.蛇床子素通过抑制磷酸二酯酶 4 减轻中性粒细胞氧化应激和失血性休克诱导的肺损伤。
Free Radic Biol Med. 2015 Dec;89:387-400. doi: 10.1016/j.freeradbiomed.2015.08.008. Epub 2015 Nov 4.
5
Toll-like receptor 4 regulates heme oxygenase-1 expression after hemorrhagic shock induced acute lung injury in mice: requirement of p38 mitogen-activated protein kinase activation.Toll样受体4调节小鼠失血性休克诱导的急性肺损伤后血红素加氧酶-1的表达：p38丝裂原活化蛋白激酶激活的必要性
Shock. 2009 May;31(5):486-92. doi: 10.1097/SHK.0b013e318188f7e1.
6
Hydroxyethyl starch 6% (130/0.4) ameliorates acute lung injury in swine hemorrhagic shock.羟乙基淀粉 6%（130/0.4）可改善猪失血性休克所致急性肺损伤。
Anesthesiology. 2010 Nov;113(5):1092-8. doi: 10.1097/ALN.0b013e3181f56029.
7
Deleterious effects of aggressive rapid crystalloid resuscitation on treatment of hyperinflammatory response and lung injury induced by hemorrhage in aging rats.积极快速晶体复苏对老龄大鼠出血诱导的过度炎症反应和肺损伤治疗的有害影响。
J Surg Res. 2014 Apr;187(2):587-95. doi: 10.1016/j.jss.2013.10.061. Epub 2013 Nov 7.
8
Calpain inhibitor I reduces the activation of nuclear factor-kappaB and organ injury/dysfunction in hemorrhagic shock.钙蛋白酶抑制剂I可减轻失血性休克时核因子-κB的激活以及器官损伤/功能障碍。
FASEB J. 2001 Jan;15(1):171-186. doi: 10.1096/fj.99-0645com.
9
Critical role of toll-like receptor 4 in hypoxia-inducible factor 1α activation during trauma/hemorrhagic shocky induced acute lung injury after lymph infusion in mice.Toll样受体4在小鼠创伤/失血性休克诱导的急性肺损伤淋巴管输注后缺氧诱导因子1α激活中的关键作用。
Shock. 2014 Sep;42(3):271-8. doi: 10.1097/SHK.0000000000000212.
10
Influence of sex and age on morphological organ damage after hemorrhagic shock.性别和年龄对失血性休克后器官形态损伤的影响。
Shock. 2008 Jun;29(6):670-4. doi: 10.1097/shk.0b013e31815c3ea0.
引用本文的文献
1
Toll-Like Receptor 4 (TLR4) and AMPK Relevance in Cardiovascular Disease.Toll样受体4（TLR4）与AMPK在心血管疾病中的相关性
Adv Pharm Bull. 2023 Jan;13(1):36-47. doi: 10.34172/apb.2023.004. Epub 2021 Oct 10.
2
Plant polysaccharides with anti-lung injury effects as a potential therapeutic strategy for COVID-19.具有抗肺损伤作用的植物多糖作为COVID-19的一种潜在治疗策略。
Front Pharmacol. 2022 Oct 20;13:982893. doi: 10.3389/fphar.2022.982893. eCollection 2022.
3
Metformin Attenuates Silica-Induced Pulmonary Fibrosis by Activating Autophagy the AMPK-mTOR Signaling Pathway.二甲双胍通过激活自噬的AMPK-mTOR信号通路减轻二氧化硅诱导的肺纤维化。
Front Pharmacol. 2021 Aug 9;12:719589. doi: 10.3389/fphar.2021.719589. eCollection 2021.
4
Metabolic Communication and Healthy Aging: Where Should We Focus Our Energy?代谢通讯与健康老龄化：我们应该把精力集中在哪里？
Dev Cell. 2020 Jul 20;54(2):196-211. doi: 10.1016/j.devcel.2020.06.011. Epub 2020 Jul 2.
5
PGC1α repression in IPF fibroblasts drives a pathologic metabolic, secretory and fibrogenic state.IPF 成纤维细胞中 PGC1α 的抑制导致病理性代谢、分泌和纤维生成状态。
Thorax. 2019 Aug;74(8):749-760. doi: 10.1136/thoraxjnl-2019-213064. Epub 2019 Jun 10.
本文引用的文献
1
Age-Dependent Changes in AMPK Metabolic Pathways in the Lung in a Mouse Model of Hemorrhagic Shock.失血性休克小鼠模型中肺脏AMPK代谢途径的年龄依赖性变化
Am J Respir Cell Mol Biol. 2017 May;56(5):585-596. doi: 10.1165/rcmb.2016-0118OC.
2
Activation of AMPK attenuates LPS-induced acute lung injury by upregulation of PGC1α and SOD1.腺苷酸活化蛋白激酶（AMPK）的激活通过上调过氧化物酶体增殖物激活受体γ辅激活因子1α（PGC1α）和超氧化物歧化酶1（SOD1）减轻脂多糖（LPS）诱导的急性肺损伤。
Exp Ther Med. 2016 Sep;12(3):1551-1555. doi: 10.3892/etm.2016.3465. Epub 2016 Jun 17.
3
Regulation and function of AMPK in physiology and diseases.AMPK在生理和疾病中的调节作用及功能
Exp Mol Med. 2016 Jul 15;48(7):e245. doi: 10.1038/emm.2016.81.
4
Sirt1 and the Mitochondria.沉默调节蛋白1与线粒体
Mol Cells. 2016 Feb;39(2):87-95. doi: 10.14348/molcells.2016.2318. Epub 2016 Feb 2.
5
Neutrophil-Derived MMP-8 Drives AMPK-Dependent Matrix Destruction in Human Pulmonary Tuberculosis.中性粒细胞衍生的基质金属蛋白酶-8驱动人类肺结核中依赖AMPK的基质破坏。
PLoS Pathog. 2015 May 21;11(5):e1004917. doi: 10.1371/journal.ppat.1004917. eCollection 2015 May.
6
Advanced age is associated with worsened outcomes and a unique genomic response in severely injured patients with hemorrhagic shock.高龄与严重创伤失血性休克患者的预后恶化及独特的基因组反应相关。
Crit Care. 2015 Mar 4;19(1):77. doi: 10.1186/s13054-015-0788-x.
7
High CO2 levels cause skeletal muscle atrophy via AMP-activated kinase (AMPK), FoxO3a protein, and muscle-specific Ring finger protein 1 (MuRF1).高二氧化碳水平通过AMP激活蛋白激酶（AMPK）、叉头转录因子O3a（FoxO3a）蛋白和肌肉特异性泛素连接酶1（MuRF1）导致骨骼肌萎缩。
J Biol Chem. 2015 Apr 3;290(14):9183-94. doi: 10.1074/jbc.M114.625715. Epub 2015 Feb 17.
8
Role of AMP-Activated Protein Kinase (AMPK) in Smoking-Induced Lung Inflammation and Emphysema.AMP激活蛋白激酶（AMPK）在吸烟诱导的肺部炎症和肺气肿中的作用
Tuberc Respir Dis (Seoul). 2015 Jan;78(1):8-17. doi: 10.4046/trd.2015.78.1.8. Epub 2015 Jan 29.
9
Adenosine monophosphate-activated protein kinase is required for pulmonary artery smooth muscle cell survival and the development of hypoxic pulmonary hypertension.一磷酸腺苷激活蛋白激酶对于肺动脉平滑肌细胞的存活和低氧性肺动脉高压的发展是必需的。
Am J Respir Cell Mol Biol. 2013 Oct;49(4):609-18. doi: 10.1165/rcmb.2012-0446OC.
10
Integrative analysis of complex cancer genomics and clinical profiles using the cBioPortal.利用 cBioPortal 进行复杂癌症基因组学和临床特征的综合分析
Sci Signal. 2013 Apr 2;6(269):pl1. doi: 10.1126/scisignal.2004088.
Zotero 插件