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Generation of a Chronic Obstructive Pulmonary Disease Model in Mice by Repeated Ozone Exposure
Published on: August 25, 2017
Reactive Oxygen Species in COPD-Related Vascular Remodeling
Li Zuo1, Chia-Chen Chuang2, Alexander D Clark2
1Molecular Physiology and Rehabilitation Research Laboratory, Radiologic Sciences and Respiratory Therapy Division, School of Health and Rehabilitation Sciences, The Ohio State University College of Medicine, The Ohio State University Wexner Medical Center, Columbus, OH, 43210, USA. zuo.4@osu.edu.
Abstract:
The pathogenesis of chronic obstructive pulmonary disease (COPD) is a multifaceted process involving the alteration of pulmonary vasculature. Such vascular remodeling can be associated with inflammation, shear stress, and hypoxia-conditions commonly seen in patients with lung diseases. Particularly, the overproduction of reactive oxygen species (ROS) in the diseased lungs contributes greatly to pulmonary vascular remodeling. ROS play an important role in vascular homeostasis, yet excessive ROS can alter pulmonary vasculature and impair lung function, as implicated in COPD at all stages. Increased inflammatory cell infiltration and endothelial dysfunction both correspond to the severity of COPD. As a byproduct of vascular remodeling, pulmonary hypertension negatively affects the long-term survival rate of COPD patients. While there is currently no cure for COPD, several treatment options have focused on alleviating COPD symptoms. Interventions such as long-term oxygen therapy, endothelium-targeted treatment, and pharmacological therapies show promising results in improving the life span of COPD patients and attenuating the progression of pulmonary hypertension. In this chapter, we aim to discuss the contributing factors of pulmonary vascular remodeling in COPD with an emphasis on the ROS, as well as potential redox treatments for COPD-related vascular remodeling.
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