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dc.contributor.authorAghapour, Mahyar
dc.contributor.authorRemels, Alexander H V
dc.contributor.authorPouwels, Simon D
dc.contributor.authorBruder, Dunja
dc.contributor.authorHiemstra, Pieter S
dc.contributor.authorCloonan, Suzanne M
dc.contributor.authorHeijink, Irene H
dc.date.accessioned2022-05-05T13:04:06Z
dc.date.available2022-05-05T13:04:06Z
dc.date.issued2019-11-06
dc.date.submitted2022-05-05
dc.identifier.pmid31693390
dc.identifier.doi10.1152/ajplung.00329.2019
dc.identifier.urihttp://hdl.handle.net/10033/623175
dc.description.abstractDisturbances in mitochondrial structure and function in lung epithelial cells have been implicated in the pathogenesis of various lung diseases, including chronic obstructive pulmonary disease (COPD). Such disturbances affect not only cellular energy metabolism but also alter a range of indispensable cellular homeostatic functions in which mitochondria are known to be involved. These range from cellular differentiation, cell death pathways, and cellular remodeling to physical barrier function and innate immunity, all of which are known to be impacted by exposure to cigarette smoke and have been linked to COPD pathogenesis. Next to their well-established role as the first physical frontline against external insults, lung epithelial cells are immunologically active. Malfunctioning epithelial cells with defective mitochondria are unable to maintain homeostasis and respond adequately to further stress or injury, which may ultimately shape the phenotype of lung diseases. In this review, we provide a comprehensive overview of the impact of cigarette smoke on the development of mitochondrial dysfunction in the lung epithelium and highlight the consequences for cell function, innate immune responses, epithelial remodeling, and epithelial barrier function in COPD. We also discuss the applicability and potential therapeutic value of recently proposed strategies for the restoration of mitochondrial function in the treatment of COPD.en_US
dc.language.isoenen_US
dc.rightsAttribution 4.0 International*
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.subjectCOPDen_US
dc.subjectcigarette smokeen_US
dc.subjectlung epithelial cellsen_US
dc.subjectmitochondrial dysfunctionen_US
dc.titleMitochondria: at the crossroads of regulating lung epithelial cell function in chronic obstructive pulmonary disease.en_US
dc.typeArticleen_US
dc.identifier.eissn1522-1504
dc.identifier.journalAmerican journal of physiology. Lung cellular and molecular physiologyen_US
dc.source.volume318
dc.source.issue1
dc.source.beginpageL149
dc.source.endpageL164
refterms.dateFOA2022-05-05T13:04:07Z
dc.source.journaltitleAmerican journal of physiology. Lung cellular and molecular physiology
dc.source.countryUnited States


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Attribution 4.0 International
Except where otherwise noted, this item's license is described as Attribution 4.0 International