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

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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

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Abstract

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

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Abstract

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