The role of calcium in hypoxia-induced signal transduction and gene expression

Mammalian cells require a constant supply of oxygen in order to maintain adequate energy production, which is essential for maintaining normal function and for ensuring cell survival. Sustained hypoxia can result in cell death. Sophisticated mechanisms have therefore evolved which allow cells to res...

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Bibliographic Details
Published in:Cell calcium (Edinburgh) 2004-09, Vol.36 (3), p.331-340
Main Authors: Seta, Karen A, Yuan, Yong, Spicer, Zachary, Lu, Gang, Bedard, James, Ferguson, Tsuneo K, Pathrose, Peterson, Cole-Strauss, Allyson, Kaufhold, Alexa, Millhorn, David E
Format: Article
Language:English
Subjects:
Animals
Calcium
Calcium - physiology
Calcium Signaling - physiology
Cell Hypoxia - physiology
Gene Expression Regulation - physiology
Humans
Hypoxia
Oxygen-sensing cells
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Summary:Mammalian cells require a constant supply of oxygen in order to maintain adequate energy production, which is essential for maintaining normal function and for ensuring cell survival. Sustained hypoxia can result in cell death. Sophisticated mechanisms have therefore evolved which allow cells to respond and adapt to hypoxia. Specialized oxygen-sensing cells have the ability to detect changes in oxygen tension and transduce this signal into organ system functions that enhance the delivery of oxygen to tissue in a wide variety of different organisms. An increase in intracellular calcium levels is a primary response of many cell types to hypoxia/ischemia. The response to hypoxia is complex and involves the regulation of multiple signaling pathways and coordinated expression of perhaps hundreds of genes. This review discusses the role of calcium in hypoxia-induced regulation of signal transduction pathways and gene expression. An understanding of the molecular events initiated by changes in intracellular calcium will lead to the development of therapeutic approaches toward the treatment of hypoxic/ischemic diseases and tumors.
ISSN:0143-4160
1532-1991
DOI:10.1016/j.ceca.2004.02.006