ArticleMitochondrion2020
Calcium overload decreases net free radical emission in cardiac mitochondria.
Article in Mitochondrion, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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The trial behind it
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Who cites it
11 citing papers in PubMed, 23 citations in OpenAlex.
- A perspective on the future of heart failure research.Journal of molecular and cellular cardiology plus · 2026Article
- Calcium signaling hypothesis: A non-negligible pathogenesis in Alzheimer's disease.Journal of advanced research · 2025Review
- NR3C1/GLMN-Mediated FKBP12.6 Ubiquitination Disrupts Calcium Homeostasis and Impairs Mitochondrial Quality Control in Stress-Induced Myocardial Damage.International journal of molecular sciences · 2025Article
- Postnatal growth restriction alters myocardial mitochondrial energetics in mice.Experimental physiology · 2024Article
- Crosstalk between adenine nucleotide transporter and mitochondrial swelling: experimental and computational approaches.Cell biology and toxicology · 2023Article
- Calcium Overload and Mitochondrial Metabolism.Biomolecules · 2022Review
- Modeling the Effects of Calcium Overload on Mitochondrial Ultrastructural Remodeling.Applied sciences (Basel, Switzerland) · 2021Article
- Identifying Site-Specific Superoxide and Hydrogen Peroxide Production Rates From the Mitochondrial Electron Transport System Using a Computational Strategy.Function (Oxford, England) · 2021Article
- Computationally modeling mammalian succinate dehydrogenase kinetics identifies the origins and primary determinants of ROS production.The Journal of biological chemistry · 2020Article
- Mesenchymal Stem/Stromal Cell-Mediated Mitochondrial Transfer and the Therapeutic Potential in Treatment of Neurological Diseases.Stem cells international · 2020Review
- Evaluation of Indigo carmine on hepatic ischemia and reperfusion injury.Acta cirurgica brasileira · 2020Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Elevated calcium and reactive oxygen species (ROS) are responsible for the bulk of cell death occurring in a variety of clinical settings that include acute coronary events, cerebrovascular accidents, and acute kidney injury. It is commonly believed that calcium and ROS participate in a viscous cycle during these events. However, the precise feedback mechanisms are unknown. We quantitatively demonstrate in this study that, on the contrary, calcium does not stimulate free radical production but suppresses it. Isolated mitochondria from guinea pig hearts were energized with a variety of substrates and exposed to calcium concentrations designed to induce moderate calcium overload conditions associated with ischemia/reperfusion injury but do not elicit the well-known mitochondrial permeability transition phenomenon. Metabolic function and free radical emission were simultaneously quantified using high-resolution respirometry and fluorimetry. Membrane potential, high amplitude swelling, and calcium dynamics were also quantified in parallel. Our results reveal that calcium overload does not lead to excessive ROS emission but does decrease ADP stimulated respiration rates for NADH-dependent pathways. Moreover, we developed an empirical model of mitochondrial free radical homeostasis to identify the processes that are different for each substrate and calcium condition. In summary, we show that in healthy guinea pig mitochondria, calcium uptake and free radical generation do not contribute to a viscous cycle and that the relationship between net free radical production and oxygen concentration is hyperbolic. Altogether, these results lay out an important foundation necessary to quantitatively determine the role of calcium in IR injury and ROS production.
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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.