Acute Cellular Oxygen Sensing in the Heart - A Role for Mitochondria?

Author: Livia C. Hool

Source: Vascular Disease Prevention, Volume 1, Number 3, November 2004 , pp. 197-206(10)

Publisher: Bentham Science Publishers

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Abstract:

Oxygen occupies a key role in cellular metabolism and function. Oxygen delivery to cells is crucial and a lack of oxygen such as occurs during myocardial infarction can be lethal. Cells must therefore be able to respond to changes in oxygen tension. Since the first studies examining the acute cellular effect of hypoxia on activation of transmitter release from glomus or type I chemoreceptor cells, it is now known that virtually all cells are able to respond to changes in oxygen tension. Despite advances made in characterising hypoxic responses, the identity of the oxygen sensor remains debated. Recently, more evidence has evolved as to how cardiac myocytes sense acute changes in oxygen. This review will examine the available evidence in support of acute oxygen sensing mechanisms with special reference to the heart. Further understanding these cellular processes should lead to interventions that assist in preventing the deleterious effects of acute changes in oxygen tension such as alterations in contractile function and cardiac arrhythmia.

Keywords: hypoxia; cellular oxygen tension; myocardial infarction; cardiac arrhythmia; oxygen sensor; hypoxia; polycythemia; HIF-1; haeme protein; oxidative phosphorylation

Document Type: Review article

DOI: http://dx.doi.org/10.2174/1567270043404854

Affiliations: 1: Physiology M311 School of Biomedical and Chemical Sciences The University of Western Australia Stirling Highway Crawley, WA 6009, Australia.

Publication date: 2004-11-01

More about this publication?
  • Vascular Disease Prevention publishes reviews as well as original papers to update all those concerned with this topic at the clinical or scientific level. In addition to clinically relevant topics, we consider reviews and original papers dealing with the more scientific aspects of vascular disease prevention. This includes the evaluation of emerging vascular risk factors, research dealing with the pathogenesis of atherosclerosis and the investigation of new treatment options both at the clinical and scientific level (e.g. epidemiology, patient-based studies, experimental models, in vitro experiments or molecular research). Therefore, another function of Vascular Disease Prevention is to bridge the gap between clinical practice and ongoing laboratory-based research.

    In particular, we welcome critical reviews and comments on recent trials. This is a topic that requires regular updates because of the large number of trials published every year.

    Debates are encouraged in the correspondence section of this journal.
    The editorial structure of Vascular Disease Prevention is set up with the aim of dealing with the submitted material as rapidly as possible. Specialist editors will provide a more expert and rapid assessment unlike a more centralized editorial structure.
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