Literature DB >> 11181957

Cellular mechanism of oxygen sensing.

J Lopez-Barneo1, R Pardal, P Ortega-Sáenz.   

Abstract

O2 sensing is a fundamental biological process necessary for adaptation of living organisms to variable habitats and physiological situations. Cellular responses to hypoxia can be acute or chronic. Acute responses rely mainly on O2-regulated ion channels, which mediate adaptive changes in cell excitability, contractility, and secretory activity. Chronic responses depend on the modulation of hypoxia-inducible transcription factors, which determine the expression of numerous genes encoding enzymes, transporters and growth factors. O2-regulated ion channels and transcription factors are part of a widely operating signaling system that helps provide sufficient O2 to the tissues and protect the cells against damage due to O2 deficiency. Despite recent advances in the molecular characterization of O2-regulated ion channels and hypoxia-inducible factors, several unanswered questions remain regarding the nature of the O2 sensor molecules and the mechanisms of interaction between the sensors and the effectors. Current models of O2 sensing are based on either a heme protein capable of reversibly binding O2 or the production of oxygen reactive species by NAD(P)H oxidases and mitochondria. Complete molecular characterization of the hypoxia signaling pathways will help elucidate the differential sensitivity to hypoxia of the various cell types and the gradation of the cellular responses to variable levels of PO2. A deeper understanding of the cellular mechanisms of O2 sensing will facilitate the development of new pharmacological tools effective in the treatment of diseases such as stroke or myocardial ischemia caused by localized deficits of O2.

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Year:  2001        PMID: 11181957     DOI: 10.1146/annurev.physiol.63.1.259

Source DB:  PubMed          Journal:  Annu Rev Physiol        ISSN: 0066-4278            Impact factor:   19.318


  140 in total

1.  Mitochondria and oxygen sensing: fueling the controversy.

Authors:  Jeremy P T Ward
Journal:  J Physiol       Date:  2003-03-07       Impact factor: 5.182

2.  Upregulation of transcription factor NRF2-mediated oxidative stress response pathway in rat brain under short-term chronic hypobaric hypoxia.

Authors:  Niroj Kumar Sethy; Manjulata Singh; Rajesh Kumar; Govindasamy Ilavazhagan; Kalpana Bhargava
Journal:  Funct Integr Genomics       Date:  2010-10-05       Impact factor: 3.410

3.  Modulation of exercise-induced spinal loop properties in response to oxygen availability.

Authors:  Thomas Rupp; Sébastien Racinais; Aurélien Bringard; Thomas Lapole; Stéphane Perrey
Journal:  Eur J Appl Physiol       Date:  2014-11-01       Impact factor: 3.078

4.  cDNA microarray analysis of changes in gene expression induced by neuronal hypoxia in vitro.

Authors:  K Jin; X O Mao; M W Eshoo; G del Rio; R Rao; D Chen; R P Simon; D A Greenberg
Journal:  Neurochem Res       Date:  2002-10       Impact factor: 3.996

5.  Differential regulation of the slow and rapid components of guinea-pig cardiac delayed rectifier K+ channels by hypoxia.

Authors:  Livia C Hool
Journal:  J Physiol       Date:  2003-11-21       Impact factor: 5.182

Review 6.  Physiological and pathological responses to hypoxia.

Authors:  Carine Michiels
Journal:  Am J Pathol       Date:  2004-06       Impact factor: 4.307

Review 7.  High altitude hypoxia: an intricate interplay of oxygen responsive macroevents and micromolecules.

Authors:  S Sarkar; P K Banerjee; W Selvamurthy
Journal:  Mol Cell Biochem       Date:  2003-11       Impact factor: 3.396

8.  A possible dual site of action for carbon monoxide-mediated chemoexcitation in the rat carotid body.

Authors:  C Barbé; F Al-Hashem; A F Conway; E Dubuis; C Vandier; P Kumar
Journal:  J Physiol       Date:  2002-09-15       Impact factor: 5.182

9.  A novel O2-sensing mechanism in rat glossopharyngeal neurones mediated by a halothane-inhibitable background K+ conductance.

Authors:  Verónica A Campanucci; Ian M Fearon; Colin A Nurse
Journal:  J Physiol       Date:  2003-03-14       Impact factor: 5.182

10.  The mitochondrial SDHD gene is required for early embryogenesis, and its partial deficiency results in persistent carotid body glomus cell activation with full responsiveness to hypoxia.

Authors:  José I Piruat; C Oscar Pintado; Patricia Ortega-Sáenz; Marta Roche; José López-Barneo
Journal:  Mol Cell Biol       Date:  2004-12       Impact factor: 4.272

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