ArticleAmerican journal of cardiovascular disease2016
Critical role of mitochondrial ROS is dependent on their site of production on the electron transport chain in ischemic heart.
Article in American journal of cardiovascular disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 71 citations in OpenAlex.
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- Protective effects of 4-methylumbelliferone on myocardial ischemia/reperfusion injury in rats through inhibition of oxidative stress and downregulation of TLR4/NF-κB/NLRP3 signaling pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Aging-induced mitochondrial dysfunction: two distinct populations of mitochondria versus a combined population.American journal of physiology. Heart and circulatory physiology · 2024Article
- Calpain inhibition decreases oxidative stress via mitochondrial regulation in a swine model of chronic myocardial ischemia.Free radical biology & medicine · 2023Article
- Succinate-mediated reactive oxygen species production in the anoxia-tolerant epaulette (Biology letters · 2023Article
- Mitofilin Heterozygote Mice Display an Increase in Myocardial Injury and Inflammation after Ischemia/Reperfusion.Antioxidants (Basel, Switzerland) · 2023Article
- A Brief Review of Low-Level Light Therapy in Depression Disorder.Journal of lasers in medical sciences · 2023Review
- Influence of sex on global myocardial ischemia tolerance and mitochondrial function in circulatory death donor hearts.American journal of physiology. Heart and circulatory physiology · 2023Article
- Effect of statin treatment on metabolites, lipids and prostanoids in patients with Statin Associated Muscle Symptoms (SAMS).PloS one · 2023Article
- Reversing mitochondrial defects in aged hearts: role of mitochondrial calpain activation.American journal of physiology. Cell physiology · 2022Article
- A narrative review of research advances in hypoxic pulmonary hypertension.Annals of translational medicine · 2022Review
- Biomarkers of Oxidative Stress Tethered to Cardiovascular Diseases.Oxidative medicine and cellular longevity · 2022Review
- Inhibition of mitochondrial respiration has fundamentally different effects on proliferation, cell survival and stress response in immature versus differentiated cardiomyocyte cell lines.Frontiers in cell and developmental biology · 2022Article
- Therapeutic Targets for Regulating Oxidative Damage Induced by Ischemia-Reperfusion Injury: A Study from a Pharmacological Perspective.Oxidative medicine and cellular longevity · 2022Review
- Ketone BodyOxidative medicine and cellular longevity · 2022Article
- Protective effects of safranal on hypoxia/reoxygenation-induced injury in H9c2 cardiac myoblasts via the PI3K/AKT/GSK3β signaling pathway.Experimental and therapeutic medicine · 2021Article
- 10-Gingerol alleviates hypoxia/reoxygenation-induced cardiomyocyte injury through inhibition of the Wnt5a/Frizzled-2 pathway.Food science & nutrition · 2021Article
- Implications of Oxidative and Nitrosative Post-Translational Modifications in Therapeutic Strategies against Reperfusion Damage.Antioxidants (Basel, Switzerland) · 2021Review
- Idebenone Ameliorates Rotenone-Induced Parkinson's Disease in Rats Through Decreasing Lipid Peroxidation.Neurochemical research · 2021Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Reactive oxygen species (ROS) generation has been implicated in many pathologies including ischemia/reperfusion (I/R) injury. This led to multiple studies on antioxidant therapies to treat cardiovascular diseases but paradoxically, results have so far been mixed as ROS production can be beneficial as a signaling mechanism and in cardiac protection via preconditioning interventions. We investigated whether the differential impact of increased ROS in injury as well as in protection could be explained by their site of production on the mitochondrial electron transport chain. Using amplex red to measure ROS production, we found that mitochondria isolated from hearts after I/R produced more ROS than non-ischemic when complex I substrate (glutamate/malate) was used. Interestingly, the substrates of complex II (succinate) and ubiquinone (sn-glycerol 3-phosphate, G3P) produced less ROS in mitochondria from I/R hearts compared to normal healthy hearts. The inhibitors of complex I (rotenone) and complex III (antimycin A) increased ROS production when glutamate/malate and G3P were used; in contrast, they reduced ROS production when the complex II substrate was used. Mitochondrial calcium retention capacity required to induce mitochondrial permeability transition pore (mPTP) opening was measured using calcium green fluorescence and was found to be higher when mitochondria were treated with G3P and succinate compared to glutamate/malate. Furthermore, Langendorff hearts treated with glutamate/malate exhibited reduced cardiac functional recovery and increased myocardial infarct size compared to hearts treated with G3P. Thus, ROS production by the stimulated respiratory chain complexes I and III has opposite roles: cardio-deleterious when produced in complex I and cardio-protective when produced in complex III. The mechanism of these ROS involves the inhibition of the mPTP opening, a key event in cell death following ischemia/reperfusion injury.
Indexed as
Identifiers
27679744PMC5030389W2525940465What OpenQuestion holds
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.