ReviewPharmaceutics2023
Potential Roles of Melatonin in Doxorubicin-Induced Cardiotoxicity: From Cellular Mechanisms to Clinical Application.
Review in Pharmaceutics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- 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
- Melatonergic Modulation of SIRT1-Nrf2 Signaling Protects Against Doxorubicin-Induced Hepatic Injury in Rats.Biomedicines · 2026Article
- Alteration of cardiac energetics and mitochondrial function in doxorubicin‑induced cardiotoxicity: Molecular mechanism and prospective implications (Review).International journal of molecular medicine · 2025Review
- Ovarian cancer and the heart: pathophysiology, chemotherapy-induced cardiotoxicity, and new therapeutic strategies.Journal of ovarian research · 2025Review
- Cardiomyopathies and a brief insight into DOX-induced cardiomyopathy.The Egyptian heart journal : (EHJ) : official bulletin of the Egyptian Society of Cardiology · 2025Review
- Melatonin mitigates doxorubicin induced chemo brain in a rat model in a NRF2/p53-SIRT1 dependent pathway.Heliyon · 2024Article
- Primary Protection of Diosmin Against Doxorubicin Cardiotoxicity via Inhibiting Oxido-Inflammatory Stress and Apoptosis in Rats.Cell biochemistry and biophysics · 2024Article
- DL-3-Heliyon · 2024Article
- Article
- Melatonin mitigates oxidative damage induced by anthracycline: a systematic-review and meta-analysis of murine models.Frontiers in cardiovascular medicine · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Doxorubicin is a potent chemotherapeutic drug; however, its clinical application has been limited due to its cardiotoxicity. One of the major mechanisms of doxorubicin-induced cardiotoxicity is the induction of oxidative stress. Evidence from in vitro and in vivo studies demonstrates that melatonin attenuated the increase in ROS production and lipid peroxidation from doxorubicin. Melatonin has been shown to exert protective effects on mitochondria damaged by doxorubicin via attenuating the depolarization of the mitochondrial membrane, restoring ATP production, and maintaining mitochondrial biogenesis. Doxorubicin increased mitochondrial fragmentation which impaired mitochondrial function; however, these adverse effects were reversed by melatonin. Melatonin also modulated cell death pathways by suppressing apoptotic and ferroptotic cell death caused by doxorubicin. These beneficial effects of melatonin could be responsible for the attenuation of changes in ECG, left ventricular dysfunction, and hemodynamic deterioration caused by doxorubicin. Despite these potential benefits, clinical evidence regarding the impact of melatonin in reducing cardiotoxicity induced by doxorubicin is still limited. Further clinical studies are justified to evaluate the efficacy of melatonin in protecting against doxorubicin-induced cardiotoxicity. This valuable information can be used to warrant the use of melatonin in a clinical setting under this condition.
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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.