ArticleJournal of molecular and cellular cardiology2008
Glutathione oxidation as a trigger of mitochondrial depolarization and oscillation in intact hearts.
Article in Journal of molecular and cellular cardiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed, 91 citations in OpenAlex.
- Mitochondrial network remodeling of the diabetic heart: implications to ischemia related cardiac dysfunction.Cardiovascular diabetology · 2024Review
- Characterization of the far-red fluorescent probe MitoView 633 for dynamic mitochondrial membrane potential measurement.Frontiers in physiology · 2023Article
- Extracellular Vesicles fromInternational journal of molecular sciences · 2022Article
- Synthesis of a fluorinated pyronin that enables blue light to rapidly depolarize mitochondria.RSC medicinal chemistry · 2022Article
- Review
- Hydrogen peroxide diffusion and scavenging shapes mitochondrial network instability and failure by sensitizing ROS-induced ROS release.Scientific reports · 2020Article
- Dysregulated metabolic pathways in age-related macular degeneration.Scientific reports · 2020Article
- Diabetes Increases the Vulnerability of the Cardiac Mitochondrial Network to Criticality.Frontiers in physiology · 2020Article
- Mitochondrial chaotic dynamics: Redox-energetic behavior at the edge of stability.Scientific reports · 2018Article
- Mitochondrial membrane potential.Analytical biochemistry · 2018Review
- Article
- Assessing Spatiotemporal and Functional Organization of Mitochondrial Networks.Methods in molecular biology (Clifton, N.J.) · 2018Article
- New and revisited approaches to preserving the reperfused myocardium.Nature reviews. Cardiology · 2017Review
- Reactive oxygen species production induced by pore opening in cardiac mitochondria: The role of complex III.The Journal of biological chemistry · 2017Article
- Reactive oxygen species production induced by pore opening in cardiac mitochondria: The role of complex II.The Journal of biological chemistry · 2017Article
- Expert consensus document: Mitochondrial function as a therapeutic target in heart failure.Nature reviews. Cardiology · 2017Review
- Functional Implications of Cardiac Mitochondria Clustering.Advances in experimental medicine and biology · 2017Review
- Computational properties of mitochondria in T cell activation and fate.Open biology · 2016Review
- Mitochondrial Flash: Integrative Reactive Oxygen Species and pH Signals in Cell and Organelle Biology.Antioxidants & redox signaling · 2016Review
- Exercise-induced protection against reperfusion arrhythmia involves stabilization of mitochondrial energetics.American journal of physiology. Heart and circulatory physiology · 2016Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Depolarization of the mitochondrial inner membrane potential (DeltaPsi(m)) associated with oxidative stress is thought to be a critical factor in cardiac dysfunction and cell injury following ischemia-reperfusion or exposure to cardiotoxic agents. In isolated cardiomyocytes, mitochondrially-generated reactive oxygen species (ROS) can readily trigger cell-wide collapse or oscillations of DeltaPsi(m) but it is not known whether these phenomena scale to the level of the whole heart. Here we utilize two-photon laser scanning fluorescence microscopy to track DeltaPsi(m), ROS, and reduced glutathione (GSH) levels in intact perfused guinea-pig hearts subjected to simulated ischemia reperfusion or GSH depletion with the thiol oxidizing agent diamide. Exposure to oxidative stress by either method provoked heterogeneous DeltaPsi(m) depolarization and occasional oscillation in clusters of myocytes in the epicardium in association with increased mitochondrial ROS production. Furthermore, the whole-heart oxidative stress dramatically increased the sensitivity of seemingly quiescent cells to DeltaPsi(m) depolarization induced by a localized laser flash. These effects were directly correlated with depletion of the intracellular GSH pool. Unexpectedly, hearts perfused with nominally Ca2+-free solution or those switched from 0.5 mM Ca2+ to nominally Ca2+-free solution also displayed heterogeneous DeltaPsi(m) depolarization and oscillation, in parallel with net oxidation of the GSH pool. The findings demonstrate that metabolic heterogeneity initiated by mitochondrial ROS-induced ROS release is present in the intact heart, and that the redox state of the glutathione pool is a key determinant of loss of DeltaPsi(m).
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.