ArticleJournal of molecular and cellular cardiology2011
Dynamic modulation of Ca2+ sparks by mitochondrial oscillations in isolated guinea pig cardiomyocytes under oxidative stress.
Article in Journal of molecular and cellular cardiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 71 citations in OpenAlex.
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- Ameliorative effects of HGF-overexpressed exosomes derived from ADMSCs on oxidative stress in hepatic fibrosis.Histology and histopathology · 2025Article
- Status of Mitochondrial Oxidative Phosphorylation during the Development of Heart Failure.Antioxidants (Basel, Switzerland) · 2023Review
- Mitochondrial Calcium Overload Plays a Causal Role in Oxidative Stress in the Failing Heart.Biomolecules · 2023Review
- Calcium and Reactive Oxygen Species Signaling Interplays in Cardiac Physiology and Pathologies.Antioxidants (Basel, Switzerland) · 2023Review
- Characterization of the far-red fluorescent probe MitoView 633 for dynamic mitochondrial membrane potential measurement.Frontiers in physiology · 2023Article
- Attenuation Aβ1-42-induced neurotoxicity in neuronal cell by 660nm and 810nm LED light irradiation.PloS one · 2023Article
- The mitochondrial CaScientific reports · 2022Article
- Optogenetic Studies of Mitochondria.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Multiscale Modeling of the Mitochondrial Origin of Cardiac Reentrant and Fibrillatory Arrhythmias.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Mitochondrial CaJournal of molecular and cellular cardiology · 2021Review
- Mitochondrial CaJournal of molecular and cellular cardiology · 2021Review
- Mitochondrial depolarization promotes calcium alternans: Mechanistic insights from a ventricular myocyte model.PLoS computational biology · 2021Article
- Mitochondrial Contributions in the Genesis of Delayed Afterdepolarizations in Ventricular Myocytes.Frontiers in physiology · 2021Article
- A Comparative Study of Rat UrineBiology · 2020Article
- MitoQ regulates redox-related noncoding RNAs to preserve mitochondrial network integrity in pressure-overload heart failure.American journal of physiology. Heart and circulatory physiology · 2020Article
- Sodium-glucose co-transporter 2 inhibition as a mitochondrial therapy for atrial fibrillation in patients with diabetes?Cardiovascular diabetology · 2020Article
- A Spatiotemporal Ventricular Myocyte Model Incorporating Mitochondrial Calcium Cycling.Biophysical journal · 2019Article
- Precisely Control Mitochondria with Light to Manipulate Cell Fate Decision.Biophysical journal · 2019Article
- Complex Regulation of Mitochondrial Function During Cardiac Development.Journal of the American Heart Association · 2019Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Local control of Ca(2+)-induced Ca(2+) release (CICR) depends on the spatial organization of L-type Ca(2+) channels and ryanodine receptors (RyR) in the dyad. Analogously, Ca(2+) uptake by mitochondria is facilitated by their close proximity to the Ca(2+) release sites, a process required for stimulating oxidative phosphorylation during changes in work. Mitochondrial feedback on CICR is less well understood. Since mitochondria are a primary source of reactive oxygen species (ROS), they could potentially influence the cytosolic redox state, in turn altering RyR open probability. We have shown that self-sustained oscillations in mitochondrial inner membrane potential (ΔΨ(m)), NADH, ROS, and reduced glutathione (GSH) can be triggered by a laser flash in cardiomyocytes. Here, we employ this method to directly examine how acute changes in energy state dynamically influence resting Ca(2+) spark occurrence and properties. Two-photon laser scanning microscopy was used to monitor cytosolic Ca(2+) (or ROS), ΔΨ(m), and NADH (or GSH) simultaneously in isolated guinea pig cardiomyocytes. Resting Ca(2+) spark frequency increased with each ΔΨ(m) depolarization and decreased with ΔΨ(m) repolarization without affecting Ca(2+) spark amplitude or time-to-peak. Stabilization of mitochondrial energetics by pretreatment with the superoxide scavenger TMPyP, or by acute addition of 4'-chlorodiazepam, a mitochondrial benzodiazepine receptor antagonist that blocks the inner membrane anion channel, prevented or reversed, respectively, the increased spark frequency. Cyclosporine A did not block the ΔΨ(m) oscillations or prevent Ca(2+) spark modulation by ΔΨ(m). The results support the hypothesis that mitochondria exert an influential role on the redox environment of the Ca(2+) handling subsystem, with mechanistic implications for the pathophysiology of cardiac disease.
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