Abstract
Hypoxia promotes physiological processes such as energy metabolism, angiogenesis, cell proliferation, and cell viability through the transcription factor Hypoxia Inducible Factor (HIF). Hypoxia also diminishes the activity of ATP consuming processes to promote cell survival. The mechanism(s) by which hypoxia activates HIF and diminishes ATP demand are a subject of intensive research. Here we outline the model in which mitochondrial complex III regulate the activity of HIF and diminish ATP utilization processes through the increased production of ROS during hypoxia.
Original language | English (US) |
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Title of host publication | Membrane Receptors, Channels and Transporters in Pulmonary Circulation |
Editors | J.X.J Yuan, J.P.T. Ward |
Pages | 339-354 |
Number of pages | 16 |
DOIs | |
State | Published - 2010 |
Publication series
Name | Advances in Experimental Medicine and Biology |
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Volume | 661 |
ISSN (Print) | 0065-2598 |
Funding
This work was supported by grant NIH grants GM60472-06, P01HL071643-01A4 and American Heart Association grant 0350054N to N.S.C., E.L.B. and B.M.E. are supported by predoctoral training grants T32 CA09560 and T32 HL076139, respectively.
Keywords
- HIF
- Mitochondria
- Na/K ATPase
- ROS
ASJC Scopus subject areas
- General Biochemistry, Genetics and Molecular Biology