Redox Dysregulation in Aging and COPD: Role of NOX Enzymes and Implications for Antioxidant Strategies

C. Schiffers, N.L. Reynaert, E.F.M. Wouters, A. van der Vliet*

*Corresponding author for this work

Research output: Contribution to journal(Systematic) Review article peer-review

Abstract

With a rapidly growing elderly human population, the incidence of age-related lung diseases such as chronic obstructive pulmonary disease (COPD) continues to rise. It is widely believed that reactive oxygen species (ROS) play an important role in ageing and in age-related disease, and approaches of antioxidant supplementation have been touted as useful strategies to mitigate age-related disease progression, although success of such strategies has been very limited to date. Involvement of ROS in ageing is largely attributed to mitochondrial dysfunction and impaired adaptive antioxidant responses. NADPH oxidase (NOX) enzymes represent an important enzyme family that generates ROS in a regulated fashion for purposes of oxidative host defense and redox-based signalling, however, the associations of NOX enzymes with lung ageing or age-related lung disease have to date only been minimally addressed. The present review will focus on our current understanding of the impact of ageing on NOX biology and its consequences for age-related lung disease, particularly COPD, and will also discuss the implications of altered NOX biology for current and future antioxidant-based strategies aimed at treating these diseases.
Original languageEnglish
Article number1799
Number of pages30
JournalAntioxidants
Volume10
Issue number11
DOIs
Publication statusPublished - 1 Nov 2021

Keywords

  • ageing
  • COPD
  • oxidative stress
  • redox signalling
  • NADPH oxidase
  • DUOX1
  • antioxidants
  • OBSTRUCTIVE PULMONARY-DISEASE
  • AIRWAY EPITHELIAL-CELLS
  • INDUCED LUNG INFLAMMATION
  • LIFE-SPAN EXTENSION
  • OXIDATIVE STRESS
  • HYDROGEN-PEROXIDE
  • CIGARETTE-SMOKE
  • MITOCHONDRIAL DYSFUNCTION
  • THERAPEUTIC TARGET
  • SENESCENT CELLS

Cite this