ArticleThe Journal of pharmacology and experimental therapeutics2010
Long-acting phosphodiesterase-5 inhibitor tadalafil attenuates doxorubicin-induced cardiomyopathy without interfering with chemotherapeutic effect.
Article in The Journal of pharmacology and experimental therapeutics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 104 citations in OpenAlex.
- Sildenafil exposure and hemodynamic effect after Fontan surgery.Pediatric critical care medicine : a journal of the Society of Critical Care Medicine and the World Federation of Pediatric Intensive and Critical Care Societies · 2014Trial
- Therapeutic effect of Fuzheng Yixin decoction on cardiac insufficiencythe soluble guanylyl cyclase-cyclic guanosine monophosphate-protein kinase G pathway in a doxorubicin-induced dilated cardiomyopathy rat model.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2026Article
- Ovarian cancer and the heart: pathophysiology, chemotherapy-induced cardiotoxicity, and new therapeutic strategies.Journal of ovarian research · 2025Review
- Potential beneficial impacts of tadalafil on cardiovascular diseases.Journal of the Chinese Medical Association : JCMA · 2025Review
- Advancements in Phosphodiesterase 5 Inhibitors: Unveiling Present and Future Perspectives.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Phosphodiesterase-5 Inhibitors as Therapeutics for Cardiovascular Diseases: A Brief Review.Iranian journal of public health · 2023Review
- Androgen-deprivation therapy with leuprolide increases abdominal adiposity without causing cardiac dysfunction in middle-aged male mice: effect of sildenafil.American journal of physiology. Regulatory, integrative and comparative physiology · 2023Article
- Phosphodiesterase 5a Signalling in Skeletal Muscle Pathophysiology.International journal of molecular sciences · 2022Article
- The role of ivabradine in doxorubicin-induced cardiotoxicity: exploring of underlying argument.Inflammopharmacology · 2022Article
- TRPC6 N338S is a gain-of-function mutant identified in patient with doxorubicin-induced cardiotoxicity.Biochimica et biophysica acta. Molecular basis of disease · 2022Article
- Cardiomyocyte Atrophy, an Underestimated Contributor in Doxorubicin-Induced Cardiotoxicity.Frontiers in cardiovascular medicine · 2022Review
- Potential cardiotoxicity induced by Euodiae Fructus:Frontiers in pharmacology · 2022Article
- Cardiotoxicity of Anticancer Drugs: Molecular Mechanisms and Strategies for Cardioprotection.Frontiers in cardiovascular medicine · 2022Review
- Sildenafil for Primary Prevention of Anthracycline-Induced Cardiac Toxicity: A Phase I/II Randomized Clinical Trial, SILDAT-TAHA6 Trial.Cardiology research and practice · 2022Article
- Diketopiperazine-Based, Flexible Tadalafil Analogues: Synthesis, Crystal Structures and Biological Activity Profile.Molecules (Basel, Switzerland) · 2021Article
- Established and emerging therapeutic uses of PDE type 5 inhibitors in cardiovascular disease.British journal of pharmacology · 2020Review
- Cardiovascular risks and toxicity - The Achilles heel of androgen deprivation therapy in prostate cancer patients.Biochimica et biophysica acta. Reviews on cancer · 2020Review
- GATA4-targeted compound exhibits cardioprotective actions against doxorubicin-induced toxicity in vitro and in vivo: establishment of a chronic cardiotoxicity model using human iPSC-derived cardiomyocytes.Archives of toxicology · 2020Article
- Cardiac Cyclic Nucleotide Phosphodiesterases: Roles and Therapeutic Potential in Heart Failure.Cardiovascular drugs and therapy · 2020Review
- From Molecular Mechanisms to Clinical Management of Antineoplastic Drug-Induced Cardiovascular Toxicity: A Translational Overview.Antioxidants & redox signaling · 2019Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Doxorubicin (DOX) is one of the most effective anticancer drugs. However, its cardiotoxicity remains a clinical concern that severely restricts its therapeutic usage. We designed this study to investigate whether tadalafil, a long-acting phosphodiesterase-5 (PDE-5) inhibitor, protects against DOX-induced cardiotoxicity. We also sought to delineate the cellular and molecular mechanisms underlying tadalafil-induced cardioprotection. Male CF-1 outbred mice were randomized into three groups (n = 15-24/group) to receive either saline (0.2 ml i.p.), DOX (15 mg/kg, given by a single intraperitoneal injection), or tadalafil (4 mg/kg p.o. daily for 9 days) plus DOX. Left ventricular function was subsequently assessed by transthoracic echocardiography and Millar conductance catheter. Cardiac contractile function was impaired by DOX, and it was significantly improved by cotreatment with tadalafil. Tadalafil attenuated DOX-induced apoptosis and depletion of prosurvival proteins, including Bcl-2 and GATA-4, in myocardium. Cardiac oxidative stress was attenuated and antioxidant capacity was enhanced by tadalafil possibly via up-regulation of mitochondrial superoxide dismutase (MnSOD). Moreover, the tadalafil-treated group demonstrated increased cardiac cGMP level and protein kinase G (PKG) activity. Tadalafil did not interfere with the efficacy of DOX in killing human osteosarcoma cells in vitro or its antitumor effect in vivo in tumor xenograft model. We conclude that tadalafil improved left ventricular function and prevented cardiomyocyte apoptosis in DOX-induced cardiomyopathy through mechanisms involving up-regulation of cGMP, PKG activity, and MnSOD level without interfering with the chemotherapeutic benefits of DOX.
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Registered trials
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