Mitochondrial redox system, dynamics, and dysfunction in lung inflammaging and COPD.


Author: Lerner CA1, Sundar IK1, Rahman I2

Affiliation: <sup>1</sup>Department of Environmental Medicine, Lung Biology and Disease Program, University of Rochester Medical Center, Rochester, NY, USA.

<sup>2</sup>Department of Environmental Medicine, Lung Biology and Disease Program, University of Rochester Medical Center, Rochester, NY, USA. Electronic address: irfan_rahman@urmc.rochester.edu.
Conference/Journal: Int J Biochem Cell Biol.
Date published: 2016 Jul 26
Other:
  Pages: S1357-2725(16)30200-X   ,  Special Notes: doi: 10.1016/j.biocel.2016.07.026. [Epub ahead of print]   ,  Word Count: 146  
    Myriad forms of endogenous and environmental stress will disrupt mitochondrial function by impacting critical processes in mitochondrial homeostasis such as mitochondrial redox system, oxidative phosphorylation, biogenesis, and mitophagy. External stressors that interfere with the steady state activity of mitochondrial functions are generally associated with an increase in reactive oxygen species, inflammatory response, and induction of cellular senescence (inflammaging) via mitochondrial damage associated molecular patterns (DAMPS) which are the key events in the pathogenesis of chronic obstructive pulmonary disease (COPD) and its exacerbations. In this review, we highlight the primary mitochondrial quality control mechanisms that are influenced by oxidative stress/redox system, including role of mitochondria during inflammation and cellular senescence, and how mitochondrial dysfunction contributes to the pathogenesis of COPD and its exacerbations via pathogenic stimuli.



Copyright © 2016 Elsevier Ltd. All rights reserved.



KEYWORDS: Cellular senescence; DAMPs; Inflammation; Mitophagy; Oxidative phosphorylation; Redox; Telomere



PMID: 27474491  DOI: 10.1016/j.biocel.2016.07.026