The mechanisms by which mitochondrial dysfunction in chronic obstructive pulmonary disease (COPD) lead to increased oxidative stress and inflammation,

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Presentation transcript:

The mechanisms by which mitochondrial dysfunction in chronic obstructive pulmonary disease (COPD) lead to increased oxidative stress and inflammation, drivers of carcinogenesis. The mechanisms by which mitochondrial dysfunction in chronic obstructive pulmonary disease (COPD) lead to increased oxidative stress and inflammation, drivers of carcinogenesis. In COPD, there is an increase in mitochondrial damage as a result of the release of mitochondrial antiviral signalling protein (MAVS), reactive oxygen species (ROS) and mitochondrial DNA (mtDNA). Damaged mitochondria should undergo physiological degradation, mitophagy. However, in COPD, the Pink1/Parkin mitophagy pathway is disrupted and therefore mitophagy is impaired. The persisting damaged mitochondria are a source of oxidants and can induce the NLRP3 inflammasome pathway. IL: interleukin; DAMPs: damage-associated molecular patterns. Francois Ng Kee Kwong et al. Eur Respir Rev 2017;26:170040 ©2017 by European Respiratory Society