Journal
INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY
Volume 81, Issue -, Pages 294-306Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.biocel.2016.07.026
Keywords
Oxidative phosphorylation; Mitophagy; Redox; Telomere; DAMPs; Inflammation; Cellular senescence
Categories
Funding
- NIH [2R01HL085613, 3R01HL085613-07S1]
- American Lung Association [RG-305393]
- Pulmonary Training grant [T32 HL066988]
- NIEHS Environmental Health Science Center grant [P30-ES001247]
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Myriad forms of endogenous and environmental stress 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) potentially via mitochondrial damage associated molecular patterns (DAMPS). Many of these 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. (C) 2016 Elsevier Ltd. All rights reserved.
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