The DOI matches its Crossref record; 87 of the 87 references it cites were found in a registry or an index.
Hypoxia and mitochondrial oxidative metabolism
Open accessAbstract
It is now clear that mitochondrial defects are associated with a large variety of clinical phenotypes. This is the result of the mitochondria's central role in energy production, reactive oxygen species homeostasis, and cell death. These processes are interdependent and may occur under various stressing conditions, among which low oxygen levels (hypoxia) are certainly prominent. Cells exposed to hypoxia respond acutely with endogenous metabolites and proteins promptly regulating metabolic pathways, but if low oxygen levels are prolonged, cells activate adapting mechanisms, the master switch being the hypoxia-inducible factor 1 (HIF-1). Activation of this factor is strictly bound to the mitochondrial function, which in turn is related with the oxygen level. Therefore in hypoxia, mitochondria act as [O2] sensors, convey signals to HIF-1 directly or indirectly, and contribute to the cell redox potential, ion homeostasis, and energy production. Although over the last two decades cellular responses to low oxygen tension have been studied extensively, mechanisms underlying these functions are still indefinite. Here we review current knowledge of the mitochondrial role in hypoxia, focusing mainly on their role in cellular energy and reactive oxygen species homeostasis in relation with HIF-1 stabilization. In addition, we address the involvement of HIF-1 and the inhibitor protein of F1F0 ATPase in the hypoxia-induced mitochondrial autophagy.
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1 retracted
Mitochondrial Autophagy Is an HIF-1-dependent Adaptive Metabolic Response to Hypoxia
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RetractedFree radicals and antioxidants in normal physiological functions and human disease
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Cited by
Reactive Oxygen Species in Metabolic and Inflammatory Signaling
Forrester, S. J., Kikuchi, D. S., Hernandes, M. S., Xu, Q., & Griendling, K. K. (2018) · Circulation Research · doi:10.1161/circresaha.117.311401 · Cited by 2,081
The Role of Oxidative Stress and Hypoxia in Pancreatic Beta-Cell Dysfunction in Diabetes Mellitus
Gerber, P. A., & Rutter, G. A. (2017) · Antioxidants & Redox Signaling · doi:10.1089/ars.2016.6755 · Cited by 654
Cancer metabolism and the Warburg effect: the role of HIF-1 and PI3K
Courtnay, R., Ngo, D. C., Malik, N., Ververis, K., Tortorella, S. M., & Karagiannis, T. C. (2015) · Molecular Biology Reports · doi:10.1007/s11033-015-3858-x · Cited by 567
PI3K/Akt and HIF‑1 signaling pathway in hypoxia‑ischemia (Review)
Zhang, Z., Yao, L., Yang, J., Wang, Z., & Du, G. (2018) · Molecular Medicine Reports · doi:10.3892/mmr.2018.9375 · Cited by 404
Macrophage metabolism in atherosclerosis
Bories, G. F. P., & Leitinger, N. (2017) · FEBS Letters · doi:10.1002/1873-3468.12786 · Cited by 145
Metadata
- Authors
- Solaini, G., Baracca, A., Lenaz, G., & Sgarbi, G.
- Venue
- Biochimica et Biophysica Acta (BBA) - Bioenergetics
- Publisher
- Elsevier BV
- Published
- 2010-06
- Volume
- 1797
- Issue
- 6-7
- Pages
- 1171-1177
- ISSN
- 0005-2728 (ISSN-L)
- OpenAlex
- W1984060145
- Cited by
- 608
- References
- 87
- FWCI
- 4.61
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Solaini, G., Baracca, A., Lenaz, G., & Sgarbi, G. (2010). Hypoxia and mitochondrial oxidative metabolism. Biochimica et Biophysica Acta (BBA) - Bioenergetics. https://doi.org/10.1016/j.bbabio.2010.02.011
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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