ArticleAmerican journal of physiology. Heart and circulatory physiology2022
Smad3 promotes adverse cardiovascular remodeling and dysfunction in doxorubicin-treated hearts.
Article in American journal of physiology. Heart and circulatory physiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Reply to the Letter to the Editor: Current role of the pericoronary fat attenuation index in breast cancer patients undergoing chemotherapy.European radiology · 2026Article
- Sustained mesenchymal reprogramming of endothelial cells after completion of chemotherapy.Cardio-oncology (London, England) · 2025Article
- Serial assessment of coronary artery inflammation using cardiac CT in anthracycline chemotherapy for breast cancer.European radiology · 2025Article
- Early Myocardial Strain Reduction and miR-122-5p Elevation Associated with Interstitial Fibrosis in Anthracycline-Induced Cardiotoxicity.Biomedicines · 2024Article
- The Role of MicroRNAs in the Pathogenesis of Doxorubicin-Induced Vascular Remodeling.International journal of molecular sciences · 2024Review
- SMAD3 mediates the specification of human induced pluripotent stem cell-derived epicardium into progenitors for the cardiac pericyte lineage.Stem cell reports · 2024Article
- Nicotinamide Mononucleotide Supplementation Alleviates Doxorubicin-Induced Multi-Organ Fibrosis.International journal of molecular sciences · 2024Article
- Priorities in Cardio-Oncology Basic and Translational Science: GCOS 2023 Symposium Proceedings:JACC. CardioOncology · 2023Review
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Authors and funding
13 authors at 5 institutions in 1 country.
Funding
Abstract
Many anticancer therapies cause serious cardiovascular complications that degrade quality of life and cause early mortality in treated patients. Specifically, doxorubicin is known as an effective anticancer agent that causes cardiomyopathy in treated patients. There has been growing interest in defining the role of endothelial cells in cardiac damage by doxorubicin. We have shown in the present study that endothelial nuclei accumulate more intravenously administered doxorubicin than other cardiac cell types. Doxorubicin enhanced cardiac production of the transforming growth factor-β (TGF-β) ligands and nuclear translocation of phospho-Smad3 in both cultured and in vivo cardiac endothelial cells. To examine the role of the TGF-β/mothers against decapentaplegic homolog 3 (Smad3) pathway in cardiac damage by doxorubicin, we used both
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