ArticleScientific reports2021
Fenofibrate attenuates doxorubicin-induced cardiac dysfunction in mice via activating the eNOS/EPC pathway.
Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06155331 (Clinical Study to Evaluate the Possible Safety and Efficacy of Fenofibrate in the Prophylaxis of Doxorubicin Induced Cardiotoxicity in Breast Cancer Patients), which is not on this map. Cited by 13 papers.
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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.
Clinical Study to Evaluate the Possible Safety and Efficacy of Fenofibrate in the Prophylaxis of Doxorubicin Induced Cardiotoxicity in Breast Cancer Patients
Who cites it
13 citing papers in PubMed, 22 citations in OpenAlex.
- Fenofibrate attenuates doxorubicin-induced cardiotoxicity in patients with breast cancer: a randomized controlled trial.Naunyn-Schmiedeberg's archives of pharmacology · 2025Trial
- Understanding the distinct role of PI3K(p110Frontiers in cardiovascular medicine · 2026Review
- Drug Repositioning in Doxorubicin-Induced Cardiotoxicity Protection.International journal of molecular sciences · 2025Review
- Improved Therapeutic Efficacy of Doxorubicin Chemotherapy With Cannabidiol in 4T1 Mice Breast Cancer Model.Cancer medicine · 2024Article
- Cardiometabolic benefits of fenofibrate in heart failure related to obesity and diabetes.Cardiovascular diabetology · 2024Article
- SGLT2 inhibitors: role in protective reprogramming of cardiac nutrient transport and metabolism.Nature reviews. Cardiology · 2023Review
- Endothelial-to-Mesenchymal Transition: Potential Target of Doxorubicin-Induced Cardiotoxicity.American journal of cardiovascular drugs : drugs, devices, and other interventions · 2023Review
- Anti-inflammatory role of fenofibrate in treating diseases.Biomolecules & biomedicine · 2023Review
- Role of oxidative stress and inflammation-related signaling pathways in doxorubicin-induced cardiomyopathy.Cell communication and signaling : CCS · 2023Review
- Review
- Cardiotoxicity of Anticancer Drugs: Molecular Mechanisms and Strategies for Cardioprotection.Frontiers in cardiovascular medicine · 2022Review
- Endothelial-Mesenchymal Transition or Functional Tissue Regeneration - Two Outcomes of Heart Remodeling.Physiological research · 2021Review
- Pachymic Acid Attenuated Doxorubicin-Induced Heart Failure by Suppressing miR-24 and Preserving Cardiac Junctophilin-2 in Rats.International journal of molecular sciences · 2021Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endothelial progenitor cells (EPCs) improve endothelial impairment, which in turn restores endothelial function in patients with heart failure (HF). In the present study, we tested whether fenofibrate, with its anti-inflammatory and vasoprotective effects, could improve myocardial function by activating EPCs through the eNOS pathway in a doxorubicin (DOX)-induced cardiomyopathy mouse model. Wild-type mice were divided into 4 groups and treated with vehicle, DOX + saline, DOX + fenofibrate, and DOX + fenofibrate + L-NAME (N(ω)-nitro-L-arginine methyl ester). DOX-induced cardiac atrophy, myocardial dysfunction, the number of circulating EPCs and tissue inflammation were analyzed. Mice in the DOX + fenofibrate group had more circulating EPCs than those in the DOX + saline group (2% versus 0.5% of total events, respectively) after 4 weeks of treatment with fenofibrate. In addition, the inhibition of eNOS by L-NAME in vivo further abolished the fenofibrate-induced suppression of DOX-induced cardiotoxic effects. Protein assays revealed that, after DOX treatment, the differential expression of MMP-2 (matrix metalloproteinase-2), MMP-9 (matrix metalloproteinase-9), TNF-α (tumor necrosis factor-α), and NT-pro-BNP (N-terminal pro-B-type natriuretic peptide) between saline- and DOX-treated mice was involved in the progression of HF. Mechanistically, fenofibrate promotes Akt/eNOS and VEGF (vascular endothelial growth factor), which results in the activation of EPC pathways, thereby ameliorating DOX-induced cardiac toxicity.
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