ArticleScientific reports2020
Doxorubicin increases permeability of murine small intestinal epithelium and cultured T84 monolayers.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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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
10 citing papers in PubMed, 13 citations in OpenAlex.
- A systematic assessment of the short- and long-term effects of commonly used breast cancer chemotherapeutics on the gut microbiome‒blood‒brain axis of female mice.Gut microbes · 2026Article
- The mucosal-neural axis in chemotherapy-induced gastrointestinal toxicity.Oncology reviews · 2026Review
- Gut Microbiota Signatures Associate with Chemotherapy-Related Adverse Events in Breast Cancer Patients.Cancers · 2025Article
- The Gut-Heart Axis and Its Role in Doxorubicin-Induced Cardiotoxicity: A Narrative Review.Microorganisms · 2025Review
- Article
- Liraglutide Pretreatment Does Not Improve Acute Doxorubicin-Induced Cardiotoxicity in Rats.International journal of molecular sciences · 2024Article
- Role of gut microbiota in doxorubicin-induced cardiotoxicity: from pathogenesis to related interventions.Journal of translational medicine · 2024Review
- Myeloperoxidase is a critical mediator of anthracycline-induced cardiomyopathy.Basic research in cardiology · 2023Article
- Toll-like Receptor 4 Inflammatory Perspective on Doxorubicin-Induced Cardiotoxicity.Molecules (Basel, Switzerland) · 2023Review
- Intestinal Microbiota Influence Doxorubicin Responsiveness in Triple-Negative Breast Cancer.Cancers · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Enteric bacteria and/or their products are necessary for doxorubicin (DXR)-induced small intestine mucosal damage. While DXR does not induce gross loss of epithelium, others have shown elevated serum endotoxin after DXR administration. However, the mechanism of movement is unknown. We hypothesized that DXR treatment resulted in increased paracellular translocation of bacteria or bacterial products through the small intestinal epithelium. We measured permeability after DXR administration using transepithelial resistance and macromolecular flux and assessed tight junctional gene expression and protein localization both in vitro using T84 cells and ex vivo using murine jejunum. DXR treatment increased flux of 4 kDa dextrans in mouse jejenum, but increased flux of 4, 10 and 20 kDa dextrans in T84 cells. Following DXR, we observed increased permeability, both in vitro and ex vivo, independent of bacteria. DXR induced increased expression of Cldn2 and Cldn4 in murine small intestine but increased only CLDN2 expression in T84 cells. DXR treatment induced disorganization of tight junctional proteins. We conclude that DXR increases paracellular transit of small macromolecules, including bacterial products, through the epithelium, by altering expression of tight junctional components and dynamic loosening of cellular tight junctions.
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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.