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Tuberc Respir Dis (Seoul). 2016 Oct;79(4):207-213. Epub 2016 Oct 5.

A Mitochondrial Perspective of Chronic Obstructive Pulmonary Disease Pathogenesis.

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Section of Pulmonary, Critical Care and Sleep Medicine, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT, USA.
Department of Pathology, Yale University School of Medicine, New Haven, CT, USA.; Department of Genetics, Yale University School of Medicine, New Haven, CT, USA.


Chronic obstructive pulmonary disease (COPD) encompasses several clinical syndromes, most notably emphysema and chronic bronchitis. Most of the current treatments fail to attenuate severity and progression of the disease, thereby requiring better mechanistic understandings of pathogenesis to develop disease-modifying therapeutics. A number of theories on COPD pathogenesis have been promulgated wherein an increase in protease burden from chronic inflammation, exaggerated production of reactive oxygen species and the resulting oxidant injury, or superfluous cell death responses caused by enhanced cellular injury/damage were proposed as the culprit. These hypotheses are not mutually exclusive and together likely represent the multifaceted biological processes involved in COPD pathogenesis. Recent studies demonstrate that mitochondria are involved in innate immune signaling that plays important roles in cigarette smoke-induced inflammasome activation, pulmonary inflammation and tissue remodeling responses. These responses are reviewed herein and synthesized into a view of COPD pathogenesis whereby mitochondria play a central role.


Mitochondria; NLRX1 Protein, Human; Pulmonary Disease, Chronic Obstructive

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