ArticleFrontiers in physiology2018
Ranolazine Attenuates Trastuzumab-Induced Heart Dysfunction by Modulating ROS Production.
Article in Frontiers in physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
25 citing papers in PubMed, 50 citations in OpenAlex.
- Osthole attenuates trastuzumab-induced cardiotoxicity in mice by enhancing autophagy via regulating the p38MAPK/mTOR signaling pathway.Journal of traditional and complementary medicine · 2026Article
- Review
- Ranolazine as a therapeutic agent for diabetic cardiomyopathy: reducing endoplasmic reticulum stress and inflammation in type 2 diabetic rat model.BMC pharmacology & toxicology · 2025Article
- Cardio-Renal and Systemic Effects of SGLT2i Dapagliflozin on Short-Term Anthracycline and HER-2-Blocking Agent Therapy-Induced Cardiotoxicity.Antioxidants (Basel, Switzerland) · 2025Article
- Unraveling the pharmacological and therapeutic potential of Ranolazine beyond antianginal drug use: a new insight.Experimental biology and medicine (Maywood, N.J.) · 2025Review
- Ranolazine: a potential anti-metastatic drug targeting voltage-gated sodium channels.British journal of cancer · 2024Review
- Sodium-glucose cotransporter 2 inhibitor dapagliflozin prevents ejection fraction reduction, reduces myocardial and renal NF-κB expression and systemic pro-inflammatory biomarkers in models of short-term doxorubicin cardiotoxicity.Frontiers in cardiovascular medicine · 2024Article
- Acetylcholinesterase inhibition protects against trastuzumab-induced cardiotoxicity through reducing multiple programmed cell death pathways.Molecular medicine (Cambridge, Mass.) · 2023Article
- Improvement of Vascular Insulin Sensitivity by Ranolazine.International journal of molecular sciences · 2023Article
- Antioxidant Protection against Trastuzumab Cardiotoxicity in Breast Cancer Therapy.Antioxidants (Basel, Switzerland) · 2023Review
- The Molecular Mechanisms of Cardiotoxicity Induced by HER2, VEGF, and Tyrosine Kinase Inhibitors: an Updated Review.Cardiovascular drugs and therapy · 2022Review
- Cardiotoxicity of Anticancer Drugs: Molecular Mechanisms and Strategies for Cardioprotection.Frontiers in cardiovascular medicine · 2022Review
- Trastuzumab does not bind rat or mouse ErbB2/neu: implications for selection of non-clinical safety models for trastuzumab-based therapeutics.Breast cancer research and treatment · 2022Article
- Immune checkpoint inhibitor therapy increases systemic SDF-1, cardiac DAMPs Fibronectin-EDA, S100/Calgranulin, galectine-3, and NLRP3-MyD88-chemokine pathways.Frontiers in cardiovascular medicine · 2022Article
- Ranolazine: An Old Drug with Emerging Potential; Lessons from Pre-Clinical and Clinical Investigations for Possible Repositioning.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Cardiomyocyte mitochondrial dynamic-related lncRNA 1 (CMDL-1) may serve as a potential therapeutic target in doxorubicin cardiotoxicity.Molecular therapy. Nucleic acids · 2021Article
- The SGLT-2 inhibitor empagliflozin improves myocardial strain, reduces cardiac fibrosis and pro-inflammatory cytokines in non-diabetic mice treated with doxorubicin.Cardiovascular diabetology · 2021Article
- Cardiotoxicity in HER2-positive breast cancer patients.Heart failure reviews · 2021Review
- The Determining Role of Mitochondrial Reactive Oxygen Species Generation and Monoamine Oxidase Activity in Doxorubicin-Induced Cardiotoxicity.Antioxidants & redox signaling · 2021Article
- Cardiotoxicity of Epidermal Growth Factor Receptor 2-Targeted Drugs for Breast Cancer.Frontiers in pharmacology · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The ErbB2 blocker trastuzumab improves survival in oncologic patients, but can cause cardiotoxicity. The late Na+ current inhibitor ranolazine has been shown to counter experimental HF, including doxorubicin cardiotoxicity (a condition characterized by derangements in redox balance), by lowering the levels of reactive oxygen species (ROS). Since ErbB2 can modulate ROS signaling, we tested whether trastuzumab cardiotoxicity could be blunted by ranolazine via redox-mediated mechanisms. Trastuzumab decreased fractional shortening and ejection fraction in mice, but ranolazine prevented heart dysfunction when co-administered with trastuzumab. Trastuzumab cardiotoxicity was accompanied by elevations in natriuretic peptides and matrix metalloproteinase 2 (MMP2) mRNAs, which were not elevated with co-treatment with ranolazine. Trastuzumab also increased cleavage of caspase-3, indicating activation of the proapoptotic machinery. Again, ranolazine prevented this activation. Interestingly, Neonatal Rat Ventricular Myocytes (NRVMs), labeled with MitoTracker Red and treated with trastuzumab, showed only a small increase in ROS compared to baseline conditions. We then stressed trastuzumab-treated cells with the beta-agonist isoproterenol to increase workload, and we observed a significant increase of probe fluorescence, compared with cells treated with isoproterenol alone, reflecting induction of oxidative stress. These effects were blunted by ranolazine, supporting a role for
Indexed as
Identifiers
What OpenQuestion holds
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.