文献检索文档翻译深度研究
Suppr Zotero 插件Zotero 插件
邀请有礼套餐&价格历史记录

新学期,新优惠

限时优惠:9月1日-9月22日

30天高级会员仅需29元

1天体验卡首发特惠仅需5.99元

了解详情
不再提醒
插件&应用
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
高级版
套餐订阅购买积分包
AI 工具
文献检索文档翻译深度研究
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 @ 2025

肺部疾病中氧化应激的机制和后果:老龄化人口的治疗意义。

Mechanisms and consequences of oxidative stress in lung disease: therapeutic implications for an aging populace.

机构信息

Division of Pulmonary, Allergy and Critical Care and Sleep Medicine, University of Arizona , Tucson, Arizona and Southern Arizona Veterans Affairs Health Care System, Tucson, Arizona.

出版信息

Am J Physiol Lung Cell Mol Physiol. 2018 Apr 1;314(4):L642-L653. doi: 10.1152/ajplung.00275.2017. Epub 2017 Dec 14.


DOI:10.1152/ajplung.00275.2017
PMID:29351446
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5966777/
Abstract

The rapid expansion of the elderly population has led to the recent epidemic of age-related diseases, including increased incidence and mortality of chronic and acute lung diseases. Numerous studies have implicated aging and oxidative stress in the pathogenesis of various pulmonary diseases; however, despite recent advances in these fields, the specific contributions of aging and oxidative stress remain elusive. This review will discuss the consequences of aging on lung morphology and physiology, and how redox imbalance with aging contributes to lung disease susceptibility. Here, we focus on three lung diseases for which aging is a significant risk factor: acute respiratory distress syndrome (ARDS), chronic obstructive pulmonary disease (COPD), and idiopathic pulmonary fibrosis (IPF). Preclinical and clinical development for redox- and senescence-altering therapeutic strategies are discussed, as well as scientific advancements that may direct current and future therapeutic development. A deeper understanding of how aging impacts normal lung function, redox balance, and injury-repair processes will inspire the development of new therapies to prevent and/or reverse age-associated pulmonary diseases, and ultimately increase health span and longevity. This review is intended to encourage basic, clinical, and translational research that will bridge knowledge gaps at the intersection of aging, oxidative stress, and lung disease to fuel the development of more effective therapeutic strategies for lung diseases that disproportionately afflict the elderly.

摘要

人口老龄化的迅速扩张导致了与年龄相关的疾病的流行,包括慢性和急性肺部疾病的发病率和死亡率上升。大量研究表明,衰老和氧化应激与各种肺部疾病的发病机制有关;然而,尽管这些领域最近取得了进展,但衰老和氧化应激的具体贡献仍不清楚。这篇综述将讨论衰老对肺部形态和生理学的影响,以及氧化还原失衡与衰老如何导致肺部疾病易感性。在这里,我们重点关注三种衰老为重要危险因素的肺部疾病:急性呼吸窘迫综合征(ARDS)、慢性阻塞性肺疾病(COPD)和特发性肺纤维化(IPF)。讨论了针对氧化还原和衰老改变的治疗策略的临床前和临床进展,以及可能指导当前和未来治疗开发的科学进展。更深入地了解衰老如何影响正常肺功能、氧化还原平衡和损伤修复过程,将激发新疗法的开发,以预防和/或逆转与年龄相关的肺部疾病,并最终延长健康寿命。这篇综述旨在鼓励基础、临床和转化研究,弥合衰老、氧化应激和肺部疾病交叉点的知识差距,为治疗老年人中发病率较高的肺部疾病提供更有效的治疗策略。

相似文献

[1]
Mechanisms and consequences of oxidative stress in lung disease: therapeutic implications for an aging populace.

Am J Physiol Lung Cell Mol Physiol. 2017-12-14

[2]
Pulmonary Diseases and Ageing.

Subcell Biochem. 2019

[3]
Adult stem cells for chronic lung diseases.

Respirology. 2013-10

[4]
The Impacts of Cellular Senescence in Elderly Pneumonia and in Age-Related Lung Diseases That Increase the Risk of Respiratory Infections.

Int J Mol Sci. 2017-2-25

[5]
Aging and Lung Disease.

Annu Rev Physiol. 2019-11-15

[6]
Lung Diseases of the Elderly: Cellular Mechanisms.

Clin Geriatr Med. 2017-8-18

[7]
Abnormal lung aging in chronic obstructive pulmonary disease and idiopathic pulmonary fibrosis.

Am J Respir Crit Care Med. 2012-5-10

[8]
Aging and Lung Disease. Clinical Impact and Cellular and Molecular Pathways.

Ann Am Thorac Soc. 2015-12

[9]
Oxidative stress and regulation of glutathione in lung inflammation.

Eur Respir J. 2000-9

[10]
Cellular senescence and autophagy in the pathogenesis of chronic obstructive pulmonary disease (COPD) and idiopathic pulmonary fibrosis (IPF).

Respir Investig. 2016-11

引用本文的文献

[1]
Cyclodextrin-Based Nanotransporters as a Versatile Tool to Manage Oxidative Stress-Induced Lung Diseases.

Antioxidants (Basel). 2025-8-17

[2]
Ascorbic acid deficiency promotes metabolic remodeling and pulmonary fibrosis that leads to respiratory failure in Sod1 and Akr1a double-knockout mice.

Redox Biol. 2025-7-1

[3]
Suppression of NOX2-Derived Reactive Oxygen Species (ROS) Reduces Epithelial-to-MesEnchymal Transition Through Blocking SiO-Regulated JNK Activation.

Toxics. 2025-4-30

[4]
Impact of E-Cigarettes on Fetal and Neonatal Lung Development: The Influence of Oxidative Stress and Inflammation.

Antioxidants (Basel). 2025-2-25

[5]
Micro- and Nano-Plastic-Induced Adverse Health Effects on Lungs and Kidneys Linked to Oxidative Stress and Inflammation.

Life (Basel). 2025-3-3

[6]
Hydroalcoholic Sumac Extract as a Protective Agent Against X-Ray-Induced Pulmonary Fibrosis.

Rep Biochem Mol Biol. 2024-7

[7]
3,5,6,7,8,3',4'- Heptamethoxyflavonoid inhibits TGF-β1-induced epithelial-mesenchymal transition by regulating oxidative stress and autophagy through MEK/ERK/PI3K/AKT/mTOR signaling pathway.

Sci Rep. 2025-2-7

[8]
The Protective Effects of Annexin A1 in Acute Lung Injury Mediated by Nrf2.

Immun Inflamm Dis. 2025-1

[9]
Treatment of Acute and Long-COVID, Diabetes, Myocardial Infarction, and Alzheimer's Disease: The Potential Role of a Novel Nano-Compound-The Transdermal Glutathione-Cyclodextrin Complex.

Antioxidants (Basel). 2024-9-12

[10]
Oxidative stress and food as medicine.

Front Nutr. 2024-8-23

本文引用的文献

[1]
The Clinical Potential of Senolytic Drugs.

J Am Geriatr Soc. 2017-10

[2]
Senolytic drugs target alveolar epithelial cell function and attenuate experimental lung fibrosis .

Eur Respir J. 2017-8-3

[3]
Approaches for extending human healthspan: from antioxidants to healthspan pharmacology.

Essays Biochem. 2017-7-11

[4]
The Intersection of Aging Biology and the Pathobiology of Lung Diseases: A Joint NHLBI/NIA Workshop.

J Gerontol A Biol Sci Med Sci. 2017-10-12

[5]
Inhibition of Bcl-2/xl With ABT-263 Selectively Kills Senescent Type II Pneumocytes and Reverses Persistent Pulmonary Fibrosis Induced by Ionizing Radiation in Mice.

Int J Radiat Oncol Biol Phys. 2017-10-1

[6]
Klotho, an antiaging molecule, attenuates oxidant-induced alveolar epithelial cell mtDNA damage and apoptosis.

Am J Physiol Lung Cell Mol Physiol. 2017-7-1

[7]
New agents that target senescent cells: the flavone, fisetin, and the BCL-X inhibitors, A1331852 and A1155463.

Aging (Albany NY). 2017-3-8

[8]
Cellular senescence mediates fibrotic pulmonary disease.

Nat Commun. 2017-2-23

[9]
Dysregulated Nox4 ubiquitination contributes to redox imbalance and age-related severity of acute lung injury.

Am J Physiol Lung Cell Mol Physiol. 2017-3-1

[10]
miR-34a promotes fibrosis in aged lungs by inducing alveolarepithelial dysfunctions.

Am J Physiol Lung Cell Mol Physiol. 2017-3-1

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

推荐工具

医学文档翻译智能文献检索