Journal
JOURNAL OF PHYSIOLOGY-LONDON
Volume 595, Issue 8, Pages 2431-2437Publisher
WILEY
DOI: 10.1113/JP273781
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Funding
- National Institutes of Health [RO1-HL085534]
- National Institute of Aging [PO1-AG049665]
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Gases are sensed by lung cells and can activate specific intracellular signalling pathways, and thus have physiological and pathophysiological effects. Carbon dioxide (CO2), a primary product of oxidative metabolism, can be sensed by eukaryotic cells eliciting specific responses via recently identified signalling pathways. However, the physiological and pathophysiological effects of high CO2 (hypercapnia) on the lungs and specific lung cells, which are the primary site of CO2 elimination, are incompletely understood. In this review, we provide a physiological and mechanistic perspective on the effects of hypercapnia on the lungs and discuss the recent understanding of CO2 modulation of the alveolar epithelial function (lung oedema clearance), epithelial cell repair, innate immunity and airway function.
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