ArticlePloS one2019
An old medicine as a new drug to prevent mitochondrial complex I from producing oxygen radicals.
Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 49 citations in OpenAlex.
- Small-molecule-induced neuron-specific hypoxia: recapitulating developmental angiogenesis for ischemic stroke therapy.Acta pharmacologica Sinica · 2026Article
- Mitochondrial oxidative stress, calcium and dynamics in cardiac ischaemia-reperfusion injury.The Journal of physiology · 2026Review
- Modulation of Nrf2 and Mitochondrial Function: Pharmacological Implications.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Advances in Pathophysiology and Novel Therapeutic Strategies for Coronary No-Reflow Phenomenon.Biomedicines · 2025Review
- Harnessing Antioxidants in Cancer Therapy: Opportunities, Challenges, and Future Directions.Antioxidants (Basel, Switzerland) · 2025Review
- Mitochondrial Dysfunction in Cardiac Disease: The Fort Fell.Biomolecules · 2024Review
- Mitochondrial destabilization in tendinopathy and potential therapeutic strategies.Journal of orthopaedic translation · 2024Review
- Mitochondrial dysfunction: mechanisms and advances in therapy.Signal transduction and targeted therapy · 2024Review
- Targeting mitochondrial dynamics and redox regulation in cardiovascular diseases.Trends in pharmacological sciences · 2024Review
- Mitochondrial Dysfunction in Heart Failure: From Pathophysiological Mechanisms to Therapeutic Opportunities.International journal of molecular sciences · 2024Review
- Potential use of antioxidants for the treatment of chronic inflammatory diseases.Frontiers in pharmacology · 2024Review
- Connection between oxidative stress and subcellular organelle in subarachnoid hemorrhage: Novel mechanisms and therapeutic implications.CNS neuroscience & therapeutics · 2023Review
- Mitochondrial Dysfunction in Cardiac Diseases and Therapeutic Strategies.Biomedicines · 2023Review
- Mitochondrial calcium and reactive oxygen species in cardiovascular disease.Cardiovascular research · 2023Review
- Mitochondrial Dysfunction Affects the Synovium of Patients with Rheumatoid Arthritis and Osteoarthritis Differently.International journal of molecular sciences · 2022Article
- HPLC-UV Method Validation for Amobarbital and Pharmaceutical Stability Evaluation When Dispersed in a Hyaluronic Acid Hydrogel: A New Concept for Post-Traumatic Osteoarthritis Prevention.Journal of pharmaceutical sciences · 2022Article
- Activation of UCP2 by anethole trithione suppresses neuroinflammation after intracerebral hemorrhage.Acta pharmacologica Sinica · 2022Article
- Therapeutic Targets for Regulating Oxidative Damage Induced by Ischemia-Reperfusion Injury: A Study from a Pharmacological Perspective.Oxidative medicine and cellular longevity · 2022Review
- Oxidative Stress and Beta Amyloid in Alzheimer's Disease. Which Comes First: The Chicken or the Egg?Antioxidants (Basel, Switzerland) · 2021Review
- Targeting oxidative stress in disease: promise and limitations of antioxidant therapy.Nature reviews. Drug discovery · 2021Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
findingsHere, we demonstrate that OP2113 (5-(4-Methoxyphenyl)-3H-1,2-dithiole-3-thione, CAS 532-11-6), synthesized and used as a drug since 1696, does not act as an unspecific antioxidant molecule (i.e., as a radical scavenger) but unexpectedly decreases mitochondrial reactive oxygen species (ROS/H2O2) production by acting as a specific inhibitor of ROS production at the IQ site of complex I of the mitochondrial respiratory chain. Studies performed on isolated rat heart mitochondria also showed that OP2113 does not affect oxidative phosphorylation driven by complex I or complex II substrates. We assessed the effect of OP2113 on an infarct model of ex vivo rat heart in which mitochondrial ROS production is highly involved and showed that OP2113 protects heart tissue as well as the recovery of heart contractile activity. CONCLUSION / SIGNIFICANCE: This work represents the first demonstration of a drug authorized for use in humans that can prevent mitochondria from producing ROS/H2O2. OP2113 therefore appears to be a member of the new class of mitochondrial ROS blockers (S1QELs) and could protect mitochondrial function in numerous diseases in which ROS-induced mitochondrial dysfunction occurs. These applications include but are not limited to aging, Parkinson's and Alzheimer's diseases, cardiac atrial fibrillation, and ischemia-reperfusion injury.
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