Role of NADPH oxidase/ROS in pro-inflammatory mediators-induced airway and pulmonary diseases

I-Ta Lee, Chuen Mao Yang

研究成果: 雜誌貢獻評論/辯論

210 引文 (Scopus)

摘要

Reactive oxygen species (ROS) are products of normal cellular metabolism and are known to act as second messengers. Under physiological conditions, ROS participate in maintenance of cellular 'redox homeostasis' in order to protect cells against oxidative stress. In addition, regulation of redox state is important for cell activation, viability, proliferation, and organ function. However, overproduction of ROS, most frequently due to excessive stimulation of either reduced nicotinamide adenine dinucleotide phosphate (NADPH) by pro-inflammatory cytokines, such as tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) or the mitochondrial electron transport chain and xanthine oxidase, results in oxidative stress. Oxidative stress is a deleterious process that leads to airway and lung damage and consequently to several respiratory inflammatory diseases/injuries, including acute respiratory distress syndrome (ARDS), asthma, cystic fibrosis (CF), and chronic obstructive pulmonary disease (COPD). Many of the known inflammatory target proteins, such as matrix metalloproteinase-9 (MMP-9), intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), cyclooxygenase-2 (COX-2), and cytosolic phospholipase A2 (cPLA2), are associated with NADPH oxidase activation and ROS overproduction in response to pro-inflammatory mediators. Thus, oxidative stress regulates both key inflammatory signal transduction pathways and target proteins involved in airway and lung inflammation. In this review, we discuss mechanisms of NADPH oxidase/ROS in the expression of inflammatory target proteins involved in airway and lung diseases. Knowledge of the mechanisms of ROS regulation could lead to the pharmacological manipulation of antioxidants in airway and lung inflammation and injury.
原文英語
頁(從 - 到)581-590
頁數10
期刊Biochemical Pharmacology
84
發行號5
DOIs
出版狀態已發佈 - 九月 1 2012
對外發佈Yes

指紋

Pulmonary diseases
NADP
Lung Diseases
Reactive Oxygen Species
Oxidoreductases
Oxidative stress
Oxidative Stress
Oxidation-Reduction
Pneumonia
Chemical activation
Cytosolic Phospholipases A2
Signal transduction
Proteins
Vascular Cell Adhesion Molecule-1
Xanthine Oxidase
Adult Respiratory Distress Syndrome
Matrix Metalloproteinase 9
Lung Injury
Second Messenger Systems
Intercellular Adhesion Molecule-1

ASJC Scopus subject areas

  • Biochemistry
  • Pharmacology

引用此文

Role of NADPH oxidase/ROS in pro-inflammatory mediators-induced airway and pulmonary diseases. / Lee, I-Ta; Yang, Chuen Mao.

於: Biochemical Pharmacology, 卷 84, 編號 5, 01.09.2012, p. 581-590.

研究成果: 雜誌貢獻評論/辯論

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AB - Reactive oxygen species (ROS) are products of normal cellular metabolism and are known to act as second messengers. Under physiological conditions, ROS participate in maintenance of cellular 'redox homeostasis' in order to protect cells against oxidative stress. In addition, regulation of redox state is important for cell activation, viability, proliferation, and organ function. However, overproduction of ROS, most frequently due to excessive stimulation of either reduced nicotinamide adenine dinucleotide phosphate (NADPH) by pro-inflammatory cytokines, such as tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) or the mitochondrial electron transport chain and xanthine oxidase, results in oxidative stress. Oxidative stress is a deleterious process that leads to airway and lung damage and consequently to several respiratory inflammatory diseases/injuries, including acute respiratory distress syndrome (ARDS), asthma, cystic fibrosis (CF), and chronic obstructive pulmonary disease (COPD). Many of the known inflammatory target proteins, such as matrix metalloproteinase-9 (MMP-9), intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), cyclooxygenase-2 (COX-2), and cytosolic phospholipase A2 (cPLA2), are associated with NADPH oxidase activation and ROS overproduction in response to pro-inflammatory mediators. Thus, oxidative stress regulates both key inflammatory signal transduction pathways and target proteins involved in airway and lung inflammation. In this review, we discuss mechanisms of NADPH oxidase/ROS in the expression of inflammatory target proteins involved in airway and lung diseases. Knowledge of the mechanisms of ROS regulation could lead to the pharmacological manipulation of antioxidants in airway and lung inflammation and injury.

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