Oxidative stress–induced mitochondrial dysfunction drives inflammation and airway smooth muscle remodeling in patients with chronic obstructive pulmonary disease

Coen Wiegman; Charalambos Michaeloudes; Gulammehdi Haji; Priyanka Narang; Colin Clarke; Kirsty Russell; Wuping Bao; Stelios Pavlidis; Peter J. Barnes; Justin Kanerva; Anton Bittner; Navin Rao; Michael P. Murphy; Paul Kirkham; Kian Fan Chung; Ian M. Adcock; Christopher E. Brightling; Donna E. Davies; Donna K. Finch; Andrew J. Fisher; A. Gaw; Alan J. Knox; Ruth J. Mayer; Michael I. Polkey; Michael Salmon; David Singh

doi:10.1016/j.jaci.2015.01.046

Abstract

Mitochondrial dysfunction in patients with COPD is associated with excessive mitochondrial ROS levels, which contribute to enhanced inflammation and cell hyperproliferation. Targeting mitochondrial ROS represents a promising therapeutic approach in patients with COPD.

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Wiegman et al. (2015) studied this question.

synapsesocial.com/papers/69d7b8c356b4d8a54e48f6fb https://doi.org/10.1016/j.jaci.2015.01.046

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Oxidative stress–induced mitochondrial dysfunction drives inflammation and airway smooth muscle remodeling in patients with chronic obstructive pulmonary disease

Abstract

Discussion

Cite This Study

Oxidative stress–induced mitochondrial dysfunction drives inflammation and airway smooth muscle remodeling in patients with chronic obstructive pulmonary disease

Abstract

Discussion

Cite This Study

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