ArticleBMC pharmacology & toxicology2021
Mitochondrial targeted antioxidants, mitoquinone and SKQ1, not vitamin C, mitigate doxorubicin-induced damage in H9c2 myoblast: pretreatment vs. co-treatment.
Article in BMC pharmacology & toxicology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 43 citations in OpenAlex.
- Mitochondrial dysfunction and applications of mitochondrial-targeted delivery systems in atherosclerosis.Drug delivery · 2026Review
- Nutritional Prevention of Oxidative Stress-Induced Cardiotoxicity in Pediatric Cardio-Oncology: Molecular Mechanisms and Translational Perspectives-A Narrative Review.International journal of molecular sciences · 2026Review
- Mitochondrial cardiomyopathy: bridging molecular mechanisms and clinical frontiers.Nature reviews. Cardiology · 2026Review
- Peroxiredoxin Ⅲ safeguards cardiac function against doxorubicin by regulating mitochondrial quality control via HRedox biology · 2026Article
- Dysfunction of the CD38-Miro1 Axis Disrupts Astrocyte-neuron Mitochondrial Transfer in Alzheimer's Disease: Mechanisms and Therapeutic Restoration.Journal of molecular neuroscience : MN · 2026Review
- Ambiol Prevents Changes in the Functional Characteristics of Mitochondria Under Hypoxia.International journal of molecular sciences · 2026Article
- Mitochondria-driven ferroptosis in intervertebral disc degeneration: A novel target in age-related spinal diseases (Review).Experimental and therapeutic medicine · 2026Review
- Targeting metabolic reprogramming to enhance adoptive immunotherapy: emerging mechanisms and translational perspectives.Journal of translational medicine · 2026Review
- Molecular and Cellular Mechanisms of Myocardial Ischemia and Reperfusion Injury: A Narrative Review.Cells · 2026Review
- Hypoxia, ROS, and HIF Signaling in I/R Injury: Implications and Future Prospects.Antioxidants (Basel, Switzerland) · 2026Review
- Oxidative Stress and Mitochondrial Dysfunction in Cardiovascular Aging: Current Insights and Therapeutic Advances.Biomedicines · 2026Review
- Mitochondria in health and disease: cellular powerhouses, signaling centers, and drivers of dysfunction.Frontiers in cell and developmental biology · 2026Review
- Mitochondrial dysfunction-driven PANoptosis in doxorubicin-induced cardiotoxicity: mechanistic insights and intervention strategies.Frontiers in pharmacology · 2026Review
- Platelet mitochondria dysfunction in diabetes mellitus: mechanisms and therapeutic implications.Frontiers in pharmacology · 2026Review
- Heat stress-induced mitochondrial damage and its impact on leukocyte function.Journal of intensive care · 2025Review
- MitoQ Protects Against Oxidative Stress-Induced Mitochondrial Dysregulation in Human Cardiomyocytes.Journal of molecular and cellular cardiology plus · 2025Article
- Ischemic stroke and intervention strategies based on the timeline of stroke progression: Review and prospects.Acta pharmaceutica Sinica. B · 2025Review
- Vitamin C as a Cardioprotective Agent Against Doxorubicin-Induced Cardiotoxicity.Journal of the American Heart Association · 2025Review
- Mitochondrial ROS inhibition prevents doxorubicin-induced breast cancer cell migration and invasion.iScience · 2025Article
- The Application and Molecular Mechanisms of Mitochondria-Targeted Antioxidants in Chemotherapy-Induced Cardiac Injury.Current issues in molecular biology · 2025Review
Corrections and comments
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPreconditioning of the heart ameliorates doxorubicin (Dox)-induced cardiotoxicity. We tested whether pretreating cardiomyocytes by mitochondrial-targeted antioxidants, mitoquinone (MitoQ) or SKQ1, would provide better protection against Dox than co-treatment.
methodsWe investigated the dose-response relationship of MitoQ, SKQ1, and vitamin C on Dox-induced damage on H9c2 cardiomyoblasts when drugs were given concurrently with Dox (e.g., co-treatment) or 24 h prior to Dox (e.g., pretreatment). Moreover, their effects on intracellular and mitochondrial oxidative stress were evaluated by 2,7-dichlorofluorescin diacetate and MitoSOX, respectively.
resultsDox (0.5-50 μM, n = 6) dose-dependently reduced cell viability. By contrast, co-treatment of MitoQ (0.05-10 μM, n = 6) and SKQ1 (0.05-10 μM, n = 6), but not vitamin C (1-2000 μM, n = 3), significantly improved cell viability only at intermediate doses (0.5-1 μM). MitoQ (1 μM) and SKQ1 (1 μM) significantly increased cell viability to 1.79 ± 0.12 and 1.59 ± 0.08 relative to Dox alone, respectively (both p < 0.05). Interestingly, when given as pretreatment, only higher doses of MitoQ (2.5 μM, n = 9) and SKQ1 (5 μM, n = 7) showed maximal protection and improved cell viability to 2.19 ± 0.13 and 1.65 ± 0.07 relative to Dox alone, respectively (both p < 0.01), which was better than that of co-treatment. Moreover, the protective effects were attributed to the significant reduction in Dox-induced intracellular and mitochondrial oxidative stress.
conclusionThe data suggest that MitoQ and SKQ1, but not vitamin C, mitigated DOX-induced damage. Moreover, MitoQ pretreatment showed significantly higher cardioprotection than its co-treatment and SKQ1, which may be due to its better antioxidant effects.
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