Suppr超能文献

代谢重编程:香烟烟雾诱导的炎症性肺病的驱动因素。

Metabolic reprogramming: A driver of cigarette smoke-induced inflammatory lung diseases.

机构信息

Department of Internal Medicine, Division of Pulmonary and Critical Care Medicine and Center for Comparative Respiratory Biology and Medicine, University of California Davis, Davis, CA, USA; Division of Nephrology, Department of Internal Medicine, University of California Davis, Davis, CA, USA.

Department of Internal Medicine, Division of Pulmonary and Critical Care Medicine and Center for Comparative Respiratory Biology and Medicine, University of California Davis, Davis, CA, USA.

出版信息

Free Radic Biol Med. 2021 Feb 1;163:392-401. doi: 10.1016/j.freeradbiomed.2020.12.438. Epub 2020 Dec 30.

Abstract

Cigarette smoking is a well-known risk factor for pulmonary diseases, including chronic obstructive pulmonary disease (COPD), asthma and pulmonary fibrosis. Despite major progress in dissecting the mechanisms associated with disease development and progression, findings only represent one aspect of multifaceted disease. A crucial consequence of this approach is that many therapeutic treatments often fail to improve or reverse the disease state as other conditions and variables are insufficiently considered. To expand our understanding of pulmonary diseases, omics approaches, particularly metabolomics, has been emerging in the field. This strategy has been applied to identify putative biomarkers and novel mechanistic insights. In this review, we discuss metabolic profiles of patients with COPD, asthma, and idiopathic pulmonary fibrosis (IPF) with a focus on the direct effects of cigarette smoking in altering metabolic regulation. We next present cell- and animal-based experiments and point out the therapeutic potential of targeting metabolic reprogramming in inflammatory lung diseases. In addition, the obstacles in translating these findings into clinical practice, including potential adverse effects and limited pharmacological efficacy, are also addressed.

摘要

吸烟是肺部疾病的一个已知危险因素,包括慢性阻塞性肺疾病(COPD)、哮喘和肺纤维化。尽管在剖析与疾病发展和进展相关的机制方面取得了重大进展,但这些发现仅代表疾病多方面的一个方面。这种方法的一个关键后果是,许多治疗方法往往无法改善或逆转疾病状态,因为其他条件和变量考虑不足。为了扩大我们对肺部疾病的理解,组学方法,特别是代谢组学,在该领域逐渐兴起。该策略已被用于确定潜在的生物标志物和新的机制见解。在这篇综述中,我们讨论了 COPD、哮喘和特发性肺纤维化(IPF)患者的代谢特征,重点讨论了吸烟对代谢调节的直接影响。接下来,我们介绍了基于细胞和动物的实验,并指出了针对炎症性肺部疾病代谢重编程的治疗潜力。此外,还讨论了将这些发现转化为临床实践所面临的障碍,包括潜在的不良反应和有限的药理疗效。

相似文献

5
Metabolomics in chronic lung diseases.代谢组学在慢性肺部疾病中的应用。
Respirology. 2020 Feb;25(2):139-148. doi: 10.1111/resp.13530. Epub 2019 Mar 25.

引用本文的文献

本文引用的文献

1
l-Arginine supplementation in severe asthma.精氨酸补充治疗重症哮喘。
JCI Insight. 2020 Jul 9;5(13):137777. doi: 10.1172/jci.insight.137777.
8
Lipid metabolism in chronic obstructive pulmonary disease.慢性阻塞性肺疾病中的脂代谢。
Int J Chron Obstruct Pulmon Dis. 2019 May 13;14:1009-1018. doi: 10.2147/COPD.S196210. eCollection 2019.
10
Pathophysiological Mechanisms of Asthma.哮喘的病理生理机制
Front Pediatr. 2019 Mar 19;7:68. doi: 10.3389/fped.2019.00068. eCollection 2019.

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验