ArticleJournal of cellular and molecular medicine2017
Folic acid reduces doxorubicin-induced cardiomyopathy by modulating endothelial nitric oxide synthase.
Article in Journal of cellular and molecular medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 50 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
- The possible effects of folic acid and postbiotic yeast on doxorubicin-induced cardiotoxicity in rats: interactions among the gut microbiota, antioxidants, and NLrp3 activities.Journal of molecular histology · 2026Article
- eNOS Uncoupling-ER Stress-Mitochondrial Dysfunction Axis in the Development of Pulmonary Hypertension.JACC. Basic to translational science · 2026Article
- Quantitative assessment of changes in left ventricular myocardial work and energy loss in HER2-positive breast cancer patients undergoing combination therapy with chemotherapy and targeted treatment using pressure-strain loop and vector flow mapping.Quantitative imaging in medicine and surgery · 2025Article
- The role of nitric oxide and connexin 43 in the cardioprotective effects of apigenin against doxorubicin-induced cardiotoxicity in male rats.Molecular biology reports · 2025Article
- Non-Coding RNAs in the Regulation of Doxorubicin-Induced Cardiotoxicity.Biomolecules · 2025Review
- Anthracycline-Induced Cardiomyopathy in Cancer Survivors: Management and Long-Term Implications.Advances in experimental medicine and biology · 2025Review
- Review
- Hyperhomocysteinaemia Promotes Doxorubicin-Induced Cardiotoxicity in Mice.Pharmaceuticals (Basel, Switzerland) · 2023Article
- Role of oxidative stress and inflammation-related signaling pathways in doxorubicin-induced cardiomyopathy.Cell communication and signaling : CCS · 2023Review
- Fucoidan Protects against Doxorubicin-Induced Cardiotoxicity by Reducing Oxidative Stress and Preventing Mitochondrial Function Injury.International journal of molecular sciences · 2022Article
- In Vitro Toxicological Profile of Labetalol-Folic Acid/Folate Co-Administration in H9c2(2-1) and HepaRG Cells.Medicina (Kaunas, Lithuania) · 2022Article
- Homocysteine, Vitamins B6 and Folic Acid in Experimental Models of Myocardial Infarction and Heart Failure-How Strong Is That Link?Biomolecules · 2022Review
- Long-Acting Thioredoxin Ameliorates Doxorubicin-Induced Cardiomyopathy via Its Anti-Oxidative and Anti-Inflammatory Action.Pharmaceutics · 2022Article
- Oestrogenic Regulation of Mitochondrial Dynamics.International journal of molecular sciences · 2022Review
- Hyperhomocysteinemia Promotes Cardiac Hypertrophy in Hypertension.Oxidative medicine and cellular longevity · 2022Article
- Cardiomyocyte Atrophy, an Underestimated Contributor in Doxorubicin-Induced Cardiotoxicity.Frontiers in cardiovascular medicine · 2022Review
- Metabolic Therapy of Heart Failure: Is There a Future for B Vitamins?International journal of molecular sciences · 2021Review
- Noncoding RNAs in doxorubicin-induced cardiotoxicity and their potential as biomarkers and therapeutic targets.Acta pharmacologica Sinica · 2021Review
- Nutraceutical, Dietary, and Lifestyle Options for Prevention and Treatment of Ventricular Hypertrophy and Heart Failure.International journal of molecular sciences · 2021Review
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Authors and funding
14 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The use of doxorubicin (DOXO) as a chemotherapeutic drug has been hampered by cardiotoxicity leading to cardiomyopathy and heart failure. Folic acid (FA) is a modulator of endothelial nitric oxide (NO) synthase (eNOS), which in turn is an important player in diseases associated with NO insufficiency or NOS dysregulation, such as pressure overload and myocardial infarction. However, the role of FA in DOXO-induced cardiomyopathy is poorly understood. The aim of this study was to test the hypothesis that FA prevents DOXO-induced cardiomyopathy by modulating eNOS and mitochondrial structure and function. Male C57BL/6 mice were randomized to a single dose of DOXO (20 mg/kg intraperitoneal) or sham. FA supplementation (10 mg/day per oral) was started 7 days before DOXO injection and continued thereafter. DOXO resulted in 70% mortality after 10 days, with the surviving mice demonstrating a 30% reduction in stroke volume compared with sham groups. Pre-treatment with FA reduced mortality to 45% and improved stroke volume (both P < 0.05 versus DOXO). These effects of FA were underlain by blunting of DOXO-induced cardiomyocyte atrophy, apoptosis, interstitial fibrosis and impairment of mitochondrial function. Mechanistically, pre-treatment with FA prevented DOXO-induced increases in superoxide anion production by reducing the eNOS monomer:dimer ratio and eNOS S-glutathionylation, and attenuated DOXO-induced decreases in superoxide dismutase, eNOS phosphorylation and NO production. Enhancing eNOS function by restoring its coupling and subsequently reducing oxidative stress with FA may be a novel therapeutic approach to attenuate DOXO-induced cardiomyopathy.
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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.