The DOI matches its Crossref record; 54 of the 54 references it cites were found in a registry or an index.
ROS and NO trigger early preconditioning: relationship to mitochondrial KATP channel
Abstract
Reactive oxygen species (ROS) and nitric oxide (NO) are implicated in induction of ischemic preconditioning. However, the relationship between these oxidant signals and opening of the mitochondrial ATP-dependent potassium (K ATP) channel during early preconditioning is not fully understood. We observed preconditioning protection by hypoxia, exogenous H 2 O 2, or PKC activator PMA in cardiomyocytes subjected to 1-h ischemia and 3-h reperfusion. Protection was abolished by K ATP channel blocker 5-hydroxydecanoate (5-HD) in each case, indicating that these triggers must act upstream from the K ATP channel. Inhibitors of NO synthase abolished protection in preconditioned cells, suggesting that NO is also required for protection. DAF-2 fluorescence (NO sensitive) increased during hypoxic triggering. This was amplified by pinacidil and inhibited by 5-HD, indicating that NO is generated subsequent to K ATP channel activation. Exogenous NO during the triggering phase conferred protection blocked by 5-HD. Exogenous NO also restored protection abolished by 5-HD or N ω-nitro-l-arginine methyl ester in preconditioned cells. Antioxidants given during pinacidil or NO triggering abolished protection, confirming that ROS are generated by K ATP channel activation. Coadministration of H 2 O 2 and NO restored PMA-induced protection in 5-HD-treated cells, indicating that ROS and NO are required downstream from the K ATP channel. We conclude that ROS can trigger preconditioning by causing activation of the K ATP channel, which then induces generation of ROS and NO that are both required for preconditioning protection.
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“Once in a high redox state, QH• can lose its unpaired electron to O2 as all upstream redox centers are fully reduced (200).”
From Mitochondrial reactive oxygen species production in excitable cells: Modulators of mitochondrial and cell function (2009) · cites this paper as [200]
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Metadata
- Authors
- Lebuffe, G., Schumacker, P. T., Shao, Z.-H., Anderson, T., Iwase, H., & Vanden Hoek, T. L.
- Affiliations
- University of Chicago (US)
- Department of Medicine, Emergency Resuscitation Center, University of Chicago, Chicago, Illinois 60637
- Venue
- American Journal of Physiology-Heart and Circulatory Physiology
- Publisher
- American Physiological Society
- Published
- 2003-01-01
- Volume
- 284
- Issue
- 1
- Pages
- H299-H308
- ISSN
- 0363-6135 (ISSN-L)
- 1522-1539
- OpenAlex
- W2130229822
- Cited by
- 227
- References
- 54
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 2 · 2023: 2 · 2022: 1 · 2021: 1 · 2020: 2 · 2019: 4 · 2018: 5 · 2017: 9 · 2016: 4 · 2015: 6 · 2014: 8 · 2013: 7 · 2012: 10
- FWCI
- 15.08
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- American Journal of Physiology-Heart and Circulatory Physiology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Ischemia and Reperfusion
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
- Keywords
- ischemic preconditioning, reactive oxygen species, nitric oxide, mitochondrial ATP-dependent potassium channel, ATP-sensitive potassium channels, cardiomyocytes, hypoxia, hydrogen peroxide, protein kinase C, 5-hydroxydecanoate, nitric oxide synthase, antioxidants, myocardial ischemia-reperfusion injury, cardioprotection
- MeSH terms
- Adenosine Triphosphate, Animals, Cells, Cultured, Chick Embryo, Hydrogen Peroxide, Mitochondria, Heart, Nitric Oxide, Protein Kinase C, Potassium Channels, Oxidants, Reactive Oxygen Species, Ischemic Preconditioning, Myocardial, Myocytes, Cardiac
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