상위피인용논문
충남대학교
HEE SUN PARK,1 SO RI KIM2 AND YONG CHUL LEE2
1Department of Internal Medicine, Chungnam National University Medical School, Daejeon, and 2Departmentof Internal Medicine, Airway Remodeling Laboratory, Chonbuk National University Medical School, Jeonju, Korea
Correspondence: Yong Chul Lee
Abstract
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 through various redox‐regulatory mechanisms. Overproduction of ROS, most frequently due to excessive stimulation of either reduced nicotinamide adenine dinucleotide phosphate by cytokines or the mitochondrial electron transport chain and xanthine oxidase, results in oxidative stress. Oxidative stress is a deleterious process that leads to lung damage and consequently to various disease states. Knowledge of the mechanisms of ROS regulation could lead to the pharmacological manipulation of antioxidants in lung inflammation and injury.
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