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J Physiol Volume 548, Number 3, 664-, May 1, 2003 DOI: 10.1113/jphysiol.2003.042168
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J Physiol (2003), 548.3, p.664
© Copyright 2003 The Physiological Society
DOI: 10.1113/jphysiol.2003.042168

Mitochondria and oxygen sensing: fuelling the controversy

Jeremy P. T. Ward

Department of Asthma, Allergy and Respiratory Science, GKT School of Medicine, King’s College London, London SE1 9RT, UK

The ability to sense oxygen tension is a key function of several tissues, including the carotid body and pulmonary vasculature. There is little consensus concerning the mechanisms underlying oxygen sensing, although recently there has been a resurgence of interest in the role of mitochondria. Numerous studies over many years have shown that inhibitors of mitochondrial function mimic hypoxia in the carotid body glomus cell, and similar, though less consistent, results have been reported for the pulmonary vasculature (see López-Barneo et al. 2001). This has led to the long standing hypothesis that oxygen sensing is related to disruption of electron flow through the mitochondrial electron transport chain (ETC), although there are significant differences of opinion concerning the details and sequellae of this disruption (e.g. Chandel & Schumacker, 2000; Michelakis et al. 2002).



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