ArticleBiology open2016
Cardiotoxic drugs Herceptin and doxorubicin inhibit cardiac microvascular endothelial cell barrier formation resulting in increased drug permeability.
Article in Biology open, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 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
39 citing papers in PubMed, 78 citations in OpenAlex.
- Endothelial Transcription Factor EB Protects Against Doxorubicin-Induced Endothelial Toxicity and Cardiac Dysfunction.Circulation · 2026Article
- Sustained mesenchymal reprogramming of endothelial cells after completion of chemotherapy.Cardio-oncology (London, England) · 2025Article
- A customizable continuous and near real-time TEER platform to study anti-cancer drug toxicity in barrier tissues.Journal of pharmaceutical analysis · 2025Article
- Non-Coding RNAs in the Regulation of Doxorubicin-Induced Cardiotoxicity.Biomolecules · 2025Review
- Different Mechanisms in Doxorubicin-Induced Neurotoxicity: Impact of BRCA Mutations.International journal of molecular sciences · 2025Review
- Article
- Reevaluating Anti-Inflammatory Therapy: Targeting Senescence to Balance Anti-Cancer Efficacy and Vascular Disease.Arteriosclerosis, thrombosis, and vascular biology · 2025Review
- The Role of MicroRNAs in the Pathogenesis of Doxorubicin-Induced Vascular Remodeling.International journal of molecular sciences · 2024Review
- Complex Interplay between DNA Damage and Autophagy in Disease and Therapy.Biomolecules · 2024Review
- Anticancer drugs and cardiotoxicity: the role of cardiomyocyte and non-cardiomyocyte cells.Frontiers in cardiovascular medicine · 2024Review
- HER2-Targeted Therapy-From Pathophysiology to Clinical Manifestation: A Narrative Review.Journal of cardiovascular development and disease · 2023Review
- An integrative review of nonobvious puzzles of cellular and molecular cardiooncology.Cellular & molecular biology letters · 2023Review
- Endothelial-to-Mesenchymal Transition: Potential Target of Doxorubicin-Induced Cardiotoxicity.American journal of cardiovascular drugs : drugs, devices, and other interventions · 2023Review
- Article
- Smad3 promotes adverse cardiovascular remodeling and dysfunction in doxorubicin-treated hearts.American journal of physiology. Heart and circulatory physiology · 2022Article
- Optimizing combination therapy in a murine model of HER2+ breast cancer.Computer methods in applied mechanics and engineering · 2022Article
- Role of non-cardiomyocytes in anticancer drug-induced cardiotoxicity: A systematic review.iScience · 2022Review
- Article
- Review
- SIRT1 activation and its effect on intercalated disc proteins as a way to reduce doxorubicin cardiotoxicity.Frontiers in pharmacology · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Cardiotoxicity induced by anti-cancer therapeutics is a severe, and potentially fatal, adverse reaction of the heart in response to certain drugs. Current in vitro approaches to assess cardiotoxicity have focused on analysing cardiomyocytes. More recently it has become apparent that non-cardiomyocyte cells of the heart can potentially contribute to cardiotoxicity. Herceptin and doxorubicin are known to induce cardiotoxicity in the clinic. The effect of these drugs on the endothelial tight junction barrier was tested by analysing tight junction formation and zona occludens-1 (ZO-1) levels, revealing that Herceptin and doxorubicin are able to induce barrier perturbment and decrease barrier function in human cardiac microvascular endothelial cells (HCMECs) leading to increased permeability. Herceptin treatment had no effect on the tight junction barrier function in human dermal and human brain microvascular endothelial cells. HCMECs showed detectable levels of HER2 compared with the other endothelial cells suggesting that Herceptin binding to HER2 in these cells may interfere with tight junction formation. Our data suggests that doxorubicin and Herceptin can affect tight junction formation in the cardiac microvasculature leading to increased drug permeability and adverse effects on the cardiac myocytes.
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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.