The DOI matches its Crossref record; 13 of the 13 references it cites were found in a registry or an index.
Hypoxic pulmonary vasoconstriction: redox events in oxygen sensing
Abstract
Recently, the mitochondria have become the focus of attention as the site of O 2 sensing underlying hypoxic pulmonary vasoconstriction (HPV). However, two disparate models have emerged to explain how mitochondria react to a decrease in Po 2. One model proposes that a drop in Po 2 decreases the rate of mitochondrial reactive oxygen species (ROS) generation, resulting in a decrease in oxidant stress and an accumulation of reducing equivalents. The resulting shift of the cytosol to a reduced state causes the inhibition of voltage-dependent potassium channels, membrane depolarization, and the influx of calcium through voltage-gated (L-type) calcium channels. A second and opposing model suggests that hypoxia triggers a paradoxical increase in a mitochondrial-induced ROS signal. The resulting shift of the cytosol to an oxidized state triggers the release of intracellular calcium stores, recruitment of calcium channels in the plasma membrane, and activation of contraction. This article summarizes the potential involvement of a mitochondria-induced ROS signal in these two very different models.
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HIFα Targeted for VHL-Mediated Destruction by Proline Hydroxylation: Implications for O 2 Sensing
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Self-citationMitochondrial reactive oxygen species trigger hypoxia-induced transcription
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Self-citationHIF-1: mediator of physiological and pathophysiological responses to hypoxia
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Production of Reactive Oxygen Species by Mitochondria
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Cited by
Ying, W. (2008) · Antioxidants & Redox Signaling · doi:10.1089/ars.2007.1672 · Cited by 1,494
Endothelial Mitochondria: Contributing to Vascular Function and Disease
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Mitochondrial reactive oxygen species and Ca 2+ signaling
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Reactive oxygen species and the control of vascular function
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Redox regulation of responses to hypoxia and NO–cGMP signaling in pulmonary vascular pathophysiology
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Metadata
- Authors
- Waypa, G. B., & Schumacker, P. T.
- Venue
- Journal of Applied Physiology
- Publisher
- American Physiological Society
- Published
- 2005-01
- Volume
- 98
- Issue
- 1
- Pages
- 404-414
- ISSN
- 0161-7567 (ISSN-L)
- 8750-7587
- 1522-1601
- OpenAlex
- W2093382413
- Cited by
- 166
- References
- 13
- FWCI
- 13.27
- Type
- journal article
- Language
- en
- Open access
- closed
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