The DOI matches its Crossref record; 66 of the 66 references it cites were found in a registry or an index.
Cellular oxygen sensing by mitochondria: old questions, new insight
Abstract
Hypoxia elicits a variety of adaptive responses at the tissue level, at the cellular level, and at the molecular level. A physiological response to hypoxia requires the existence of an O 2 sensor coupled to a signal transduction system, which in turn activates the functional response. Although much has been learned about the signaling systems activated by hypoxia, no consensus exists regarding the nature of the underlying O 2 sensor or whether multiple sensors exist. Among previously considered mechanisms, heme proteins have been suggested to undergo allosteric modification in response to O 2 binding or release at different [Formula: see text] levels. Other studies suggest that ion channels may change conductance as a function of[Formula: see text], allowing them to signal the onset of hypoxia. Still other studies suggest that NADPH oxidase may decrease its generation of reactive O 2 species (ROS) during hypoxia. Recent data suggest that mitochondria may function as O 2 sensors by increasing their generation of ROS during hypoxia. These oxidant signals appear to act as second messengers in the adaptive responses to hypoxia in a variety of cell types. Such observations contribute to a growing awareness that mitochondria do more than just generate ATP, in that they initiate signaling cascades involved in adaptive responses to hypoxia and that they participate in the control of cell death pathways.
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Cites
1 retracted
Hypoxia-inducible Factor 1α (HIF-1α) Is a Non-heme Iron Protein
Srinivas, V., Zhu, X., Salceda, S., Nakamura, R., & Caro, J. (1998) · Journal of Biological Chemistry · doi:10.1074/jbc.273.29.18019 · Cited by 69
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Mitochondrial reactive oxygen species trigger hypoxia-induced transcription
Chandel, N. S., Maltepe, E., Goldwasser, E., Mathieu, C. E., Simon, M. C., & Schumacker, P. T. (1998) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.95.20.11715 · Cited by 1,926
Self-citationKorshunov, S. S., Skulachev, V. P., & Starkov, A. A. (1997) · FEBS Letters · doi:10.1016/s0014-5793(97)01159-9 · Cited by 1,727
Human Cells Lacking mtDNA: Repopulation with Exogenous Mitochondria by Complementation
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RESPIRATORY ENZYMES IN OXIDATIVE PHOSPHORYLATION
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Cited by
Hypoxia, HIF1 and glucose metabolism in the solid tumour
Denko, N. C. (2008) · Nature Reviews Cancer · doi:10.1038/nrc2468 · Cited by 1,707
HIF-1 and human disease: one highly involved factor
Semenza, G. L. (2000) · Genes & Development · doi:10.1101/gad.14.16.1983 · Cited by 909
Stowe, D. F., & Camara, A. K. S. (2009) · Antioxidants & Redox Signaling · doi:10.1089/ars.2008.2331 · Cited by 471
González-Alonso, J., Olsen, D. B., & Saltin, B. (2002) · Circulation Research · doi:10.1161/01.res.0000044939.73286.e2 · Cited by 331
Dada, L. A., Chandel, N. S., Ridge, K. M., Pedemonte, C., Bertorello, A. M., & Sznajder, J. I. (2003) · Journal of Clinical Investigation · doi:10.1172/jci200316826 · Cited by 314
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Metadata
- Authors
- Chandel, N. S., & Schumacker, P. T.
- Venue
- Journal of Applied Physiology
- Publisher
- American Physiological Society
- Published
- 2000-05-01
- Volume
- 88
- Issue
- 5
- Pages
- 1880-1889
- ISSN
- 0161-7567 (ISSN-L)
- 8750-7587
- 1522-1601
- OpenAlex
- W2120649642
- Cited by
- 391
- References
- 66
- FWCI
- 11.21
- Type
- journal article
- Language
- en
- Open access
- closed
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
