Mitochondrial regulation of oxygen sensing
Abstract
Maintenance of oxygen homoeostasis is required for the survival of higher organisms. The transcription factor hypoxia inducible factor (HIF) has a crucial role in oxygen homoeostasis by integrating the decrease in oxygen levels to increase hypoxic gene expression. How cells sense decrease in oxygen levels to elicit an increase in HIF dependent gene expression is not fully understood. In this review, we discuss the role of mitochondria as oxygen sensors regulating HIF.
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Although nonmitochondrial sources of ROS exist during ischemia, the majority of ROS are likely derived from the mitochondrial respiratory complexes.
“Although nonmitochondrial sources of ROS exist during ischemia [e.g., NAD(P)H oxidase (141, 188, 328) and xanthine oxidase (25) in vasculature], the majority of ROS are likely derived from the mitochondrial respiratory complexes, as shown by the damage to respiratory complexes (212, 213, 245) and the effect of mitochondrial inhibitors (5, 28, 71, 81–86).”
From Mitochondrial reactive oxygen species production in excitable cells: Modulators of mitochondrial and cell function (2009) · cites this paper as [28]
Leakage of electrons from complexes I and III of the electron transport chain generates the superoxide ion, which is converted to hydrogen peroxide; hydrogen peroxide can diffuse out of the organelle and stabilize HIFs.
“Leakage of electrons from the complexes of the electron transport chain, in particular complexes I and III, generates the superoxide ion, which is then converted to hydrogen peroxide.Being non-polar hydrogen peroxide diffuses out of the organelle and can stabilize HIFs (48).”
From Placental Origins of Chronic Disease (2016) · cites this paper as [48]
The metabolic intermediate 2-oxoglutarate generated in the tricarboxylic acid cycle is a co-factor regulating PHD activity.
“In addition, the metabolic intermediate 2-oxoglutarate generated in the tricarboxylic acid cycle is a co-factor regulating PHD activity (48).”
From Placental Origins of Chronic Disease (2016) · cites this paper as [48]
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References 71 · Cited by 130
- Authors
- Bell, E. L., Emerling, B. M., & Chandel, N. S.
- Affiliations
- Northwestern University (US)
- Corresponding author
- Chandel, Navdeep S.
- Venue
- Mitochondrion
- Publisher
- Elsevier BV
- Published
- 2005-10
- Volume
- 5
- Issue
- 5
- Pages
- 322-332
- ISSN
- 1567-7249 (ISSN-L)
- OpenAlex
- W3022059932
- Cited by
- 130
- References
- 71
- Citations by year
- 2026: 1 · 2023: 5 · 2022: 5 · 2021: 2 · 2020: 2 · 2019: 4 · 2018: 2 · 2017: 4 · 2016: 7 · 2015: 7 · 2014: 5 · 2013: 8 · 2012: 4
- FWCI
- 1.17
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Mitochondrion (publishedVersion)
- PubMed (publishedVersion)
- Funders
- American Heart Association
- National Institutes of Health
- National Heart, Lung, and Blood Institute (P01HL071643, T32HL076139)
- National Cancer Institute (T32 CA09560, T32CA009560)
- National Institute of General Medical Sciences (GM60472-06, R01GM060472)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Neuroscience of respiration and sleep
- Keywords
- hypoxia-inducible factor, oxygen homeostasis, hypoxic gene expression, mitochondrial respiration
- MeSH terms
- Animals, Hypoxia, Electron Transport, Gene Expression Regulation, Homeostasis, Humans, Mitochondria, Models, Biological, Neovascularization, Pathologic, Oxygen, Signal Transduction, Reactive Oxygen Species, Hypoxia-Inducible Factor 1
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