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Thorax 2004;59:90-92; doi:10.1136/thorax.2003.017020
Copyright © 2004 BMJ Publishing Group Ltd & British Thoracic Society.
Thorax 2004;59:90-92
© 2004 BMJ Publishing Group Ltd & British Thoracic Society

EDITORIAL

Oxygen sensing

New insights into oxygen sensing at a cellular level

S R Walmsley, K K K Sheares, A Sobolewski, N W Morrell, E R Chilvers

Respiratory Medicine Division, Department of Medicine, University of Cambridge School of Clinical Medicine, Addenbrooke’s and Papworth Hospitals, Cambridge, UK

Correspondence to:
Correspondence to:
Professor E Chilvers
Respiratory Medicine Division, Department of Medicine, University of Cambridge School of Clinical Medicine, Box 157, Level 5 Addenbrooke’s Hospital, Hills Road, Cambridge CB2 2QQ, UK; erc24@cam.ac.uk


The oxygen sensing pathway offers a new set of therapeutic targets for conditions ranging from inflammatory lung disease to pulmonary hypertension

Keywords: hypoxia; oxygen sensing; hypoxia inducible factor-1{alpha} (HIF-1{alpha}); prolyl hydroxylase domain containing enzymes (PHDs)

Abbreviations: ARNT, aryl hydrocarbon receptor nuclear translocator; FIH, factor inhibiting HIF; HIF, hypoxia inducible factor; HRE, hypoxic response element; PHD, prolyl hydroxylase domain containing enzyme

The first 150 words of the full text of this article appear below.

The ability of cells to detect and respond to a fall in oxygen tension is of fundamental importance for maintaining oxidative metabolism and tissue homeostasis. One of the challenges facing scientists working in this area has been that any proposed mechanism for oxygen sensing has to accommodate the very different tolerances of certain tissues to hypoxia and the extreme variation in the cellular responses observed. Hence, while skeletal muscle cells can recover function after 30 minutes of anoxia, the brain suffers irreparable damage after only 4–6 minutes of ischaemia.1 Moreover, while carotid body cells respond to changes in oxygen tension that barely register in non-chemosensory tissues (and do so within seconds),2 upregulation of erythropoietin synthesis in the interstitial peritubular cells is transcriptionally regulated and requires far more protracted periods of hypoxaemia.3 Despite such variances in oxygen sensitivity and response time, all cells appear capable of responding to hypoxia . . . [Full text of this article]


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This article has been cited by other articles:

  • Siddiqui, S., Hollins, F., Saha, S., Brightling, C. E. (2007). Inflammatory cell microlocalisation and airway dysfunction: cause and effect?. Eur Respir J 30: 1043-1056 [Abstract] [Full Text]  

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