Mitochondrial redox system, dynamics, and dysfunction in lung inflammaging and COPD
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- 作者：Chad A. Lerner ; Isaac K. Sundar ; Irfan Rahman ; irfan_rahman@urmc.rochester.edu
- 关键词：AMPK ; AMP-activated protein kinase ; COPD ; chronic obstructive pulmonary disease ; COX ; cytochrome c oxidase ; CS ; cigarette smoke ; DRP1 ; DNM1L ; dynamin 1-like ; Δψm ; mitochondrial membrane potential ; ETC ; electron transport chain ; FIS1 ; fission 1 ; H2O2 ; hydrogen peroxide ; LC3 ; microtubule-associated protein light chain 3 ; MDVs ; mitochondria-derived vesicles ; Mfn ; mitofusin ; MPTP ; mitochondrial permeability transition pore ; mtDNA ; mitochondrial DNA ; mtROS ; mitochondrial reactive oxygen species ; mtDA
- 刊名：The International Journal of Biochemistry & Cell Biology
- 出版年：2016
- 出版时间：December 2016
- 年：2016
- 卷：81
- 期：part_PB
- 页码：294-306
- 全文大小：2492 K
- 卷排序：81
文摘
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.