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本文引用的文献

1
Chronic alcohol ingestion changes the landscape of the alveolar epithelium.慢性酒精摄入改变了肺泡上皮的形态。
Biomed Res Int. 2013;2013:470217. doi: 10.1155/2013/470217. Epub 2012 Dec 30.
2
Inhibition of mechanosensitive signaling in myofibroblasts ameliorates experimental pulmonary fibrosis.肌成纤维细胞中机械敏感性信号的抑制可改善实验性肺纤维化。
J Clin Invest. 2013 Mar;123(3):1096-108. doi: 10.1172/JCI66700. Epub 2013 Feb 22.
3
Role of T cells in a gp91phox knockout murine model of acute allergic asthma.T 细胞在急性过敏性哮喘 gp91phox 敲除鼠模型中的作用。
Allergy Asthma Clin Immunol. 2013 Feb 7;9(1):6. doi: 10.1186/1710-1492-9-6.
4
Role of nicotinamide adenine dinucleotide phosphate-reduced oxidase proteins in Pseudomonas aeruginosa-induced lung inflammation and permeability.烟酰胺腺嘌呤二核苷酸磷酸氧化酶蛋白在铜绿假单胞菌诱导的肺部炎症和通透性中的作用。
Am J Respir Cell Mol Biol. 2013 Apr;48(4):477-88. doi: 10.1165/rcmb.2012-0242OC.
5
NADPH oxidase and Nrf2 regulate gastric aspiration-induced inflammation and acute lung injury.NADPH 氧化酶和 Nrf2 调节胃吸入诱导的炎症和急性肺损伤。
J Immunol. 2013 Feb 15;190(4):1714-24. doi: 10.4049/jimmunol.1202410. Epub 2013 Jan 7.
6
Balancing reactive oxygen species in the epigenome: NADPH oxidases as target and perpetrator.在表观基因组中平衡活性氧物种:NADPH 氧化酶作为靶点和肇事者。
Antioxid Redox Signal. 2013 May 20;18(15):1937-45. doi: 10.1089/ars.2012.4895. Epub 2012 Nov 5.
7
NADPH-oxidase 4 protects against kidney fibrosis during chronic renal injury.NADPH-氧化酶 4 可防止慢性肾损伤过程中的肾脏纤维化。
J Am Soc Nephrol. 2012 Dec;23(12):1967-76. doi: 10.1681/ASN.2012040373. Epub 2012 Oct 25.
8
Studies of mitochondrial and nonmitochondrial sources implicate nicotinamide adenine dinucleotide phosphate oxidase(s) in the increased skeletal muscle superoxide generation that occurs during contractile activity.研究表明,在线粒体和非线粒体来源中,烟酰胺腺嘌呤二核苷酸磷酸氧化酶(s)参与了收缩活动期间骨骼肌中超氧阴离子生成的增加。
Antioxid Redox Signal. 2013 Feb 20;18(6):603-21. doi: 10.1089/ars.2012.4623. Epub 2012 Dec 6.
9
NADPH oxidase NOX4 mediates stellate cell activation and hepatocyte cell death during liver fibrosis development.NADPH 氧化酶 NOX4 在肝纤维化发展过程中介导星状细胞激活和肝细胞死亡。
PLoS One. 2012;7(9):e45285. doi: 10.1371/journal.pone.0045285. Epub 2012 Sep 26.
10
Changes in NADPH oxidase mRNA level can be detected in blood at inhaled corticosteroid treated asthmatic children.在吸入皮质类固醇治疗的哮喘儿童的血液中可以检测到 NADPH 氧化酶 mRNA 水平的变化。
Life Sci. 2012 Nov 2;91(19-20):907-11. doi: 10.1016/j.lfs.2012.08.039. Epub 2012 Sep 13.

NADPH 氧化酶在肺部健康和疾病中的作用。

NADPH oxidases in lung health and disease.

机构信息

Division of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, University of Alabama at Birmingham , Birmingham, Alabama.

出版信息

Antioxid Redox Signal. 2014 Jun 10;20(17):2838-53. doi: 10.1089/ars.2013.5608. Epub 2014 Jan 3.

DOI:10.1089/ars.2013.5608
PMID:24093231
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4026303/
Abstract

SIGNIFICANCE

The evolution of the lungs and circulatory systems in vertebrates ensured the availability of molecular oxygen (O2; dioxygen) for aerobic cellular metabolism of internal organs in large animals. O2 serves as the physiologic terminal acceptor of mitochondrial electron transfer and of the NADPH oxidase (Nox) family of oxidoreductases to generate primarily water and reactive oxygen species (ROS), respectively.

RECENT ADVANCES

The purposeful generation of ROS by Nox family enzymes suggests important roles in normal physiology and adaptation, most notably in host defense against invading pathogens and in cellular signaling.

CRITICAL ISSUES

However, there is emerging evidence that, in the context of chronic stress and/or aging, Nox enzymes contribute to the pathogenesis of a number of lung diseases.

FUTURE DIRECTIONS

Here, we review evolving functions of Nox enzymes in normal lung physiology and emerging pathophysiologic roles in lung disease.

摘要

意义

脊椎动物的肺和循环系统的进化确保了大型动物内部器官有氧细胞代谢所需的分子氧(O2;氧气)。O2 作为线粒体电子传递和 NADPH 氧化酶(Nox)家族氧化还原酶的生理末端受体,分别产生水和活性氧(ROS)。

最近的进展

Nox 家族酶有意产生 ROS,表明其在正常生理和适应中具有重要作用,尤其是在宿主防御入侵病原体和细胞信号转导方面。

关键问题

然而,越来越多的证据表明,在慢性应激和/或衰老的情况下,Nox 酶会导致多种肺部疾病的发病机制。

未来方向

在这里,我们回顾了 Nox 酶在正常肺生理学中的不断发展的功能以及在肺部疾病中的新兴病理生理作用。