• 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

当前及未来的哮喘治疗方法。

Current and future asthma therapies.

作者信息

Kandeel M, Balaha M, Inagaki N, Kitade Y

机构信息

Department of Pharmacology, Kafrelshiekh University, Kafrelshiekh, Egypt.

出版信息

Drugs Today (Barc). 2013 May;49(5):325-39. doi: 10.1358/dot.2013.49.5.1950149.

DOI:10.1358/dot.2013.49.5.1950149
PMID:23724412
Abstract

Corticosteroids (CST) are the gold standard for asthma management and for several decades have been considered the cornerstone for asthma control. With the recent advent of genomic and structural analysis technologies, the molecular basis of the side effects, toxicity and resistance mechanisms of drug treatment are better understood. With respect to CST, there is consistent evidence that while CST therapy improves asthma symptoms, it does not alter the natural course of asthma or offer clear long-lasting improvement of respiratory performance. Therefore, the development of drugs capable of minimizing or avoiding CST side effects, toxicity and resistance could be the way forward for establishing new asthma therapies. This review summarizes the molecular basis of corticosteroid mechanisms of action and the related mechanisms influencing side effects and resistance. The future of CST adjunctive or replacement therapy is also briefly discussed.

摘要

皮质类固醇(CST)是哮喘管理的金标准,几十年来一直被视为哮喘控制的基石。随着基因组和结构分析技术的最新出现,药物治疗的副作用、毒性和耐药机制的分子基础得到了更好的理解。关于CST,有一致的证据表明,虽然CST疗法可改善哮喘症状,但它不会改变哮喘的自然病程,也不能带来呼吸功能的明显持久改善。因此,开发能够最小化或避免CST副作用、毒性和耐药性的药物可能是建立新的哮喘治疗方法的前进方向。本综述总结了皮质类固醇作用机制的分子基础以及影响副作用和耐药性的相关机制。还简要讨论了CST辅助或替代疗法的未来。

相似文献

1
Current and future asthma therapies.当前及未来的哮喘治疗方法。
Drugs Today (Barc). 2013 May;49(5):325-39. doi: 10.1358/dot.2013.49.5.1950149.
2
Potential therapeutic targets for steroid-resistant asthma.治疗类固醇抵抗性哮喘的潜在靶点。
Curr Drug Targets. 2010 Aug;11(8):957-70. doi: 10.2174/138945010791591412.
3
Update on glucocorticoid action and resistance.糖皮质激素作用与抵抗的最新进展。
J Allergy Clin Immunol. 2006 Mar;117(3):522-43. doi: 10.1016/j.jaci.2006.01.032.
4
New drugs for asthma.哮喘新药物。
Semin Respir Crit Care Med. 2012 Dec;33(6):685-94. doi: 10.1055/s-0032-1326965. Epub 2012 Oct 9.
5
Mitogen-activated protein kinases as therapeutic targets for asthma.丝裂原活化蛋白激酶作为哮喘的治疗靶点。
Pharmacol Ther. 2017 Jun;174:112-126. doi: 10.1016/j.pharmthera.2017.02.024. Epub 2017 Feb 14.
6
Evaluation of combination long-acting beta-2 agonists and inhaled glucocorticosteroids for treatment of asthma.长效β2受体激动剂与吸入性糖皮质激素联合治疗哮喘的评估。
Expert Opin Drug Metab Toxicol. 2009 Aug;5(8):933-40. doi: 10.1517/17425250903127226.
7
Newer glucocorticosteroids and corticosteroid resistance reversal in asthma.新型糖皮质激素与哮喘中糖皮质激素抵抗的逆转
Pharm Pat Anal. 2013 May;2(3):373-85. doi: 10.4155/ppa.13.14.
8
Addressing corticosteroid insensitivity in adults with asthma.解决成人哮喘中的皮质类固醇不敏感问题。
Expert Rev Respir Med. 2016 Feb;10(2):137-56. doi: 10.1586/17476348.2016.1133304. Epub 2016 Jan 28.
9
Pharmacogenetics of asthma.哮喘的药物遗传学。
Curr Opin Pharmacol. 2010 Jun;10(3):226-35. doi: 10.1016/j.coph.2010.05.013.
10
[Nongenomic effects of glucocorticoids, an important mechanism of inhaled glucocorticoids action in asthma].[糖皮质激素的非基因组效应,吸入性糖皮质激素治疗哮喘的重要作用机制]
Pneumonol Alergol Pol. 2009;77(5):453-9.

引用本文的文献

1
Tolerogenic Dendritic Cells Reduce Airway Inflammation in a Model of Dust Mite Triggered Allergic Inflammation.耐受性树突状细胞在尘螨引发的变应性炎症模型中减轻气道炎症。
Allergy Asthma Immunol Res. 2018 Jul;10(4):406-419. doi: 10.4168/aair.2018.10.4.406.
2
A-kinase anchoring proteins: cAMP compartmentalization in neurodegenerative and obstructive pulmonary diseases.A激酶锚定蛋白:神经退行性疾病和阻塞性肺疾病中的环磷酸腺苷区室化
Br J Pharmacol. 2014 Dec;171(24):5603-23. doi: 10.1111/bph.12882.