ArticleJACC. CardioOncology2020
Dual Angiotensin Receptor-Neprilysin Inhibition With Sacubitril/Valsartan Attenuates Systolic Dysfunction in Experimental Doxorubicin-Induced Cardiotoxicity.
Article in JACC. CardioOncology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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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
25 citing papers in PubMed, 45 citations in OpenAlex.
- Sacubitril/Valsartan and Prevention of Cardiac Dysfunction During Adjuvant Breast Cancer Therapy: The PRADA II Randomized Clinical Trial.Circulation · 2025Trial
- Sacubitril/Valsartan for Prevention of Cancer Therapy-Related Cardiac Dysfunction: A Systematic Review and Meta-Analysis of Randomized Controlled Trials.Journal of cardiovascular development and disease · 2026Review
- Angiotensin receptor-neprilysin inhibitors improve the outcome of lung cancer patients with hypertension undergoing immune checkpoint inhibitors treatment.BMC cardiovascular disorders · 2025Article
- Inflammasomes as Potential Therapeutic Targets to Prevent Chronic Active Viral Myocarditis-Translating Basic Science into Clinical Practice.International journal of molecular sciences · 2025Review
- Sacubitril/valsartan attenuated myocardial inflammation, fibrosis, apoptosis and promoted autophagy in doxorubicin-induced cardiotoxicity mice via regulating the AMPKα-mTORC1 signaling pathway.Molecular and cellular biochemistry · 2025Article
- Doxorubicin or Epirubicin Versus Liposomal Doxorubicin Therapy-Differences in Cardiotoxicity.Cardiovascular toxicology · 2025Review
- Value of Label-Free Ubiquitin-Proteomic Analysis on Defining the Protective Mechanism of Valsartan against Doxorubicin-Induced Heart Failure.Current cancer drug targets · 2025Article
- Management of Fluoropyrimidine-Induced Cardiac Adverse Outcomes Following Cancer Treatment.Cardiovascular toxicology · 2024Review
- miScience · 2023Article
- Signaling Pathways and Potential Therapeutic Strategies in Cardiac Fibrosis.International journal of molecular sciences · 2023Review
- Review
- In Vivo Murine Models of Cardiotoxicity Due to Anticancer Drugs: Challenges and Opportunities for Clinical Translation.Journal of cardiovascular translational research · 2022Review
- Sacubitril/valsartan in Heart Failure and Beyond-From Molecular Mechanisms to Clinical Relevance.Reviews in cardiovascular medicine · 2022Review
- Sacubitril/valsartan reduces endoplasmic reticulum stress in a rat model of doxorubicin-induced cardiotoxicity.Archives of toxicology · 2022Article
- LCZ696 ameliorates doxorubicin-induced cardiomyocyte toxicity in rats.Scientific reports · 2022Article
- Novel Cardiac Computed Tomography Methods for the Assessment of Anthracycline Induced Cardiotoxicity.Frontiers in cardiovascular medicine · 2022Review
- Time to switch angiotensin-converting enzyme inhibitors/angiotensin receptor blockers to sacubitril/valsartan in patients with cancer therapy-related cardiac dysfunction.The Journal of international medical research · 2022Article
- Molecular mechanisms of sacubitril/valsartan in cardiac remodeling.Frontiers in pharmacology · 2022Review
- Novel Therapeutics for Anthracycline Induced Cardiotoxicity.Frontiers in cardiovascular medicine · 2022Review
- Multimodality Advanced Cardiovascular and Molecular Imaging for Early Detection and Monitoring of Cancer Therapy-Associated Cardiotoxicity and the Role of Artificial Intelligence and Big Data.Frontiers in cardiovascular medicine · 2022Review
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundDoxorubicin (DOX) induces cardiotoxicity in part by activation of matrix metalloproteinases (MMPs). Sacubitril/valsartan (Sac/Val) exerts additive cardioprotective actions over renin-angiotensin-aldosterone inhibitors in preclinical models of myocardial infarction and in heart failure patients. We hypothesized that Sac/Val would be more cardioprotective than Val in a rodent model of progressive DOX-induced cardiotoxicity, and this benefit would be associated with modulation of MMP activation.
objectivesWe sought to investigate the efficacy of Sac/Val for the treatment of anthracycline-induced cardiotoxicity.
methodsMale Wistar rats received DOX intraperitoneally (15 mg/kg cumulative) or saline over 3 weeks. Following the first treatment, control animals were gavaged daily with water (n = 25), while DOX-treated animals were gavaged daily with water (n = 25), Val (31 mg/kg; n = 25) or Sac/Val (68 mg/kg; n = 25) for either 4 or 6 weeks. Echocardiography was performed at baseline, and 4 and 6 weeks after DOX initiation. In addition, myocardial MMP activity was assessed with
resultsLeft ventricular ejection fraction decreased by 10% at 6 weeks in DOX and DOX + Val rats (both p < 0.05), while this reduction was attenuated in DOX + Sac/Val rats. MMP activity was increased at 6 weeks by 76% in DOX-alone rats, and tended to increase in DOX + Val rats (36%; p = 0.051) but was similar in DOX + Sac/Val rats as compared with time-matched control animals. Both therapies attenuated histological evidence of cellular toxicity and fibrosis (p < 0.05).
conclusionsSac/Val offers greater protection against left ventricular remodeling and dysfunction compared with standard angiotensin receptor blocker therapy in a rodent model of progressive DOX-induced cardiotoxicity.
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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.