• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

哮喘中的线粒体功能障碍与氧化应激:对线粒体靶向抗氧化疗法的启示

Mitochondrial Dysfunction and Oxidative Stress in Asthma: Implications for Mitochondria-Targeted Antioxidant Therapeutics.

作者信息

Reddy P Hemachandra

机构信息

Neurogenetics Laboratory, Division of Neuroscience, Oregon National Primate Research Center, Oregon Health and Science University, 505 NW 185th Avenue, Beaverton, OR 97006, USA.

出版信息

Pharmaceuticals (Basel). 2011 Feb 25;4(3):429-456. doi: 10.3390/ph4030429.

DOI:10.3390/ph4030429
PMID:21461182
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3066010/
Abstract

Asthma is a complex, inflammatory disorder characterized by airflow obstruction of variable degrees, bronchial hyper-responsiveness, and airway inflammation. Asthma is caused by environmental factors and a combination of genetic and environmental stimuli. Genetic studies have revealed that multiple loci are involved in the etiology of asthma. Recent cellular, molecular, and animal-model studies have revealed several cellular events that are involved in the progression of asthma, including: increased Th2 cytokines leading to the recruitment of inflammatory cells to the airway, and an increase in the production of reactive oxygen species and mitochondrial dysfunction in the activated inflammatory cells, leading to tissue injury in the bronchial epithelium. Further, aging and animal model studies have revealed that mitochondrial dysfunction and oxidative stress are involved and play a large role in asthma. Recent studies using experimental allergic asthmatic mouse models and peripheral cells and tissues from asthmatic humans have revealed antioxidants as promising treatments for people with asthma. This article summarizes the latest research findings on the involvement of inflammatory changes, and mitochondrial dysfunction/oxidative stress in the development and progression of asthma. This article also addresses the relationship between aging and age-related immunity in triggering asthma, the antioxidant therapeutic strategies in treating people with asthma.

摘要

哮喘是一种复杂的炎症性疾病,其特征为不同程度的气流阻塞、支气管高反应性和气道炎症。哮喘由环境因素以及遗传和环境刺激的共同作用引起。基因研究表明,多个基因座参与哮喘的病因。近期的细胞、分子和动物模型研究揭示了一些参与哮喘进展的细胞事件,包括:Th2细胞因子增加导致炎性细胞募集至气道,以及活化的炎性细胞中活性氧生成增加和线粒体功能障碍,进而导致支气管上皮组织损伤。此外,衰老和动物模型研究表明,线粒体功能障碍和氧化应激参与其中并在哮喘中起重要作用。近期使用实验性变应性哮喘小鼠模型以及哮喘患者外周细胞和组织的研究表明,抗氧化剂有望成为哮喘患者的治疗方法。本文总结了关于炎症变化、线粒体功能障碍/氧化应激在哮喘发生和发展中的作用的最新研究结果。本文还探讨了衰老及与年龄相关的免疫在引发哮喘中的关系,以及治疗哮喘患者的抗氧化治疗策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0607/4053795/7d905255c68a/pharmaceuticals-04-00429f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0607/4053795/9f10d230bbb6/pharmaceuticals-04-00429f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0607/4053795/a901db2e1267/pharmaceuticals-04-00429f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0607/4053795/53f0a7798472/pharmaceuticals-04-00429f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0607/4053795/11712045dc2c/pharmaceuticals-04-00429f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0607/4053795/7d905255c68a/pharmaceuticals-04-00429f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0607/4053795/9f10d230bbb6/pharmaceuticals-04-00429f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0607/4053795/a901db2e1267/pharmaceuticals-04-00429f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0607/4053795/53f0a7798472/pharmaceuticals-04-00429f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0607/4053795/11712045dc2c/pharmaceuticals-04-00429f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0607/4053795/7d905255c68a/pharmaceuticals-04-00429f5.jpg

相似文献

1
Mitochondrial Dysfunction and Oxidative Stress in Asthma: Implications for Mitochondria-Targeted Antioxidant Therapeutics.哮喘中的线粒体功能障碍与氧化应激:对线粒体靶向抗氧化疗法的启示
Pharmaceuticals (Basel). 2011 Feb 25;4(3):429-456. doi: 10.3390/ph4030429.
2
Molecular mechanisms of oxidative stress in asthma.哮喘中氧化应激的分子机制
Mol Aspects Med. 2022 Jun;85:101026. doi: 10.1016/j.mam.2021.101026. Epub 2021 Oct 6.
3
Oxidative and nitrative stress in bronchial asthma.支气管哮喘中的氧化应激和硝化应激
Antioxid Redox Signal. 2008 Apr;10(4):785-97. doi: 10.1089/ars.2007.1937.
4
Mitochondrial-targeted antioxidant therapy decreases transforming growth factor-β-mediated collagen production in a murine asthma model.线粒体靶向抗氧化疗法可降低小鼠哮喘模型中转化生长因子-β介导的胶原蛋白生成。
Am J Respir Cell Mol Biol. 2015 Jan;52(1):106-15. doi: 10.1165/rcmb.2013-0519OC.
5
Herbal decoction Divya-Swasari-Kwath attenuates airway inflammation and remodeling through Nrf-2 mediated antioxidant lung defence in mouse model of allergic asthma.草药煎剂迪维亚-斯瓦萨里-夸特通过 Nrf-2 介导的抗氧化肺防御减轻变应性哮喘小鼠模型中的气道炎症和重塑。
Phytomedicine. 2020 Nov;78:153295. doi: 10.1016/j.phymed.2020.153295. Epub 2020 Jul 31.
6
Vanadium exposure exacerbates allergic airway inflammation and remodeling through triggering reactive oxidative stress.钒暴露通过触发活性氧化应激加重过敏性气道炎症和重塑。
Front Immunol. 2023 Jan 11;13:1099509. doi: 10.3389/fimmu.2022.1099509. eCollection 2022.
7
Protective Effects of Licochalcone A Improve Airway Hyper-Responsiveness and Oxidative Stress in a Mouse Model of Asthma.甘草查尔酮 A 对哮喘小鼠气道高反应性和氧化应激的保护作用。
Cells. 2019 Jun 20;8(6):617. doi: 10.3390/cells8060617.
8
Effects of vitamin E on mitochondrial dysfunction and asthma features in an experimental allergic murine model.维生素E对实验性变应性小鼠模型中线粒体功能障碍和哮喘特征的影响。
J Appl Physiol (1985). 2009 Oct;107(4):1285-92. doi: 10.1152/japplphysiol.00459.2009. Epub 2009 Jul 23.
9
Mitochondrial structural changes and dysfunction are associated with experimental allergic asthma.线粒体结构变化和功能障碍与实验性变应性哮喘相关。
J Immunol. 2008 Sep 1;181(5):3540-8. doi: 10.4049/jimmunol.181.5.3540.
10
Tetrahydrocurcumin, a major metabolite of curcumin, ameliorates allergic airway inflammation by attenuating Th2 response and suppressing the IL-4Rα-Jak1-STAT6 and Jagged1/Jagged2 -Notch1/Notch2 pathways in asthmatic mice.四氢姜黄素是姜黄素的主要代谢产物,可通过减轻 Th2 反应和抑制哮喘小鼠的 IL-4Rα-Jak1-STAT6 和 Jagged1/Jagged2-Notch1/Notch2 通路来改善过敏性气道炎症。
Clin Exp Allergy. 2018 Nov;48(11):1494-1508. doi: 10.1111/cea.13258. Epub 2018 Sep 12.

引用本文的文献

1
Mitochondrial haplogroup M contributes to asthma risk in the Kuwaiti population.线粒体单倍群M与科威特人群的哮喘风险相关。
Front Allergy. 2025 Aug 8;6:1618964. doi: 10.3389/falgy.2025.1618964. eCollection 2025.
2
Bioinformatics analysis and preliminary validation of autophagy-related genes in asthma disease.哮喘疾病中自噬相关基因的生物信息学分析及初步验证
Sci Rep. 2025 Jul 1;15(1):21475. doi: 10.1038/s41598-025-08316-4.
3
PEBP1 and 15-LO-1 in Asthma: Biomarker Potential for Diagnosis and Severity Stratification.哮喘中的PEBP1和15-LO-1:诊断及严重程度分层的生物标志物潜力

本文引用的文献

1
Toxicity of neurons treated with herbicides and neuroprotection by mitochondria-targeted antioxidant SS31.用除草剂处理后的神经元毒性和线粒体靶向抗氧化剂 SS31 的神经保护作用。
Int J Environ Res Public Health. 2011 Jan;8(1):203-21. doi: 10.3390/ijerph8010203. Epub 2011 Jan 19.
2
Mitochondria-targeted antioxidants protect against amyloid-beta toxicity in Alzheimer's disease neurons.线粒体靶向抗氧化剂可预防阿尔茨海默病神经元中的淀粉样β毒性。
J Alzheimers Dis. 2010;20 Suppl 2(Suppl 2):S609-31. doi: 10.3233/JAD-2010-100564.
3
A sequence variant on 17q21 is associated with age at onset and severity of asthma.
Diagnostics (Basel). 2025 May 24;15(11):1322. doi: 10.3390/diagnostics15111322.
4
Effects of glial-derived neurotrophic factor on remodeling and mitochondrial function in human airway smooth muscle cells.胶质细胞源性神经营养因子对人呼吸道平滑肌细胞重塑和线粒体功能的影响。
Am J Physiol Lung Cell Mol Physiol. 2024 Nov 1;327(5):L684-L693. doi: 10.1152/ajplung.00101.2024. Epub 2024 Sep 24.
5
Urine metabolomics signature reveals novel determinants of adrenal suppression in children taking inhaled corticosteroids to control asthma symptoms.尿代谢组学特征揭示了儿童使用吸入性皮质类固醇控制哮喘症状时肾上腺抑制的新决定因素。
Immun Inflamm Dis. 2024 Jul;12(7):e1315. doi: 10.1002/iid3.1315.
6
Neutralization of CX3CL1 Attenuates TGF-β-Induced Fibroblast Differentiation Through NF-κB Activation and Mitochondrial Dysfunction in Airway Fibrosis.中性粒细胞趋化因子 1 抑制通过 NF-κB 激活和线粒体功能障碍的气道纤维化中的 TGF-β 诱导的成纤维细胞分化。
Lung. 2024 Jun;202(3):343-356. doi: 10.1007/s00408-024-00701-6. Epub 2024 Apr 28.
7
The role of mitochondria in eosinophil function: implications for severe asthma pathogenesis.线粒体在嗜酸性粒细胞功能中的作用:对重度哮喘发病机制的影响。
Front Cell Dev Biol. 2024 Mar 1;12:1360079. doi: 10.3389/fcell.2024.1360079. eCollection 2024.
8
Mitochondrial Dysfunction and Metabolic Reprogramming in Obesity and Asthma.肥胖与哮喘中的线粒体功能障碍和代谢重编程
Int J Mol Sci. 2024 Mar 3;25(5):2944. doi: 10.3390/ijms25052944.
9
Nuclear and mitochondrial genetic variants associated with mitochondrial DNA copy number.与线粒体 DNA 拷贝数相关的核和线粒体遗传变异。
Sci Rep. 2024 Jan 24;14(1):2083. doi: 10.1038/s41598-024-52373-0.
10
The Relationship between Fine Particle Matter (PM2.5) Exposure and Upper Respiratory Tract Diseases.细颗粒物(PM2.5)暴露与上呼吸道疾病之间的关系。
J Pers Med. 2024 Jan 16;14(1):98. doi: 10.3390/jpm14010098.
17q21 上的序列变异与哮喘的发病年龄和严重程度相关。
Eur J Hum Genet. 2010 Aug;18(8):902-8. doi: 10.1038/ejhg.2010.38. Epub 2010 Apr 7.
4
IL25 elicits a multipotent progenitor cell population that promotes T(H)2 cytokine responses.IL-25 诱导产生促进 T(H)2 细胞因子应答的多能祖细胞群体。
Nature. 2010 Apr 29;464(7293):1362-6. doi: 10.1038/nature08901. Epub 2010 Mar 3.
5
Oxidative stress and antioxidant defenses in asthmatic murine model exposed to printer emissions and environmental tobacco smoke.打印机排放物和环境烟草烟雾暴露于哮喘小鼠模型中的氧化应激和抗氧化防御。
J Environ Pathol Toxicol Oncol. 2009;28(4):325-40. doi: 10.1615/jenvironpatholtoxicoloncol.v28.i4.70.
6
MMP12, lung function, and COPD in high-risk populations.MMP12、肺功能与高危人群的 COPD。
N Engl J Med. 2009 Dec 31;361(27):2599-608. doi: 10.1056/NEJMoa0904006. Epub 2009 Dec 16.
7
Novel antioxidant approaches to the treatment of upper airway inflammation.治疗上呼吸道炎症的新型抗氧化方法。
Curr Opin Allergy Clin Immunol. 2010 Feb;10(1):34-41. doi: 10.1097/ACI.0b013e328334f613.
8
A role for Wnt signaling genes in the pathogenesis of impaired lung function in asthma.Wnt 信号基因在哮喘肺功能障碍发病机制中的作用。
Am J Respir Crit Care Med. 2010 Feb 15;181(4):328-36. doi: 10.1164/rccm.200907-1009OC. Epub 2009 Nov 19.
9
Glutathione peroxidase-2 protects from allergen-induced airway inflammation in mice.谷胱甘肽过氧化物酶-2 可保护小鼠免受过敏原诱导的气道炎症。
Eur Respir J. 2010 May;35(5):1148-54. doi: 10.1183/09031936.00026108. Epub 2009 Nov 6.
10
High dose vitamin C supplementation increases the Th1/Th2 cytokine secretion ratio, but decreases eosinophilic infiltration in bronchoalveolar lavage fluid of ovalbumin-sensitized and challenged mice.高剂量维生素 C 补充可增加卵清蛋白致敏和激发小鼠支气管肺泡灌洗液中 Th1/Th2 细胞因子分泌比值,但可减少嗜酸性粒细胞浸润。
J Agric Food Chem. 2009 Nov 11;57(21):10471-6. doi: 10.1021/jf902403p.