ArticleJournal of molecular and cellular cardiology2016
The TGF-β pathway mediates doxorubicin effects on cardiac endothelial cells.
Article in Journal of molecular and cellular cardiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 40 citations in OpenAlex.
- Doxorubicin-Induced Cardiac Remodeling: Mechanisms and Mitigation Strategies.Cardiovascular drugs and therapy · 2026Review
- Role of Perindopril in Mitigating Doxorubicin's Vascular Toxicity in a Rat Model.Cardiovascular toxicology · 2026Article
- Sustained mesenchymal reprogramming of endothelial cells after completion of chemotherapy.Cardio-oncology (London, England) · 2025Article
- Article
- METTL3-Mediated m6A Modification of ISG15 mRNA Regulates Doxorubicin-Induced Endothelial Cell Apoptosis.Journal of cellular and molecular medicine · 2025Article
- The Role of MicroRNAs in the Pathogenesis of Doxorubicin-Induced Vascular Remodeling.International journal of molecular sciences · 2024Review
- A Co-Culture System for Studying Cellular Interactions in Vascular Disease.Bioengineering (Basel, Switzerland) · 2024Review
- Doxorubicin‑induced cardiomyopathy is mitigated by empagliflozin via the modulation of endoplasmic reticulum stress pathways.Molecular medicine reports · 2024Article
- Article
- Endothelial-to-Mesenchymal Transition: Potential Target of Doxorubicin-Induced Cardiotoxicity.American journal of cardiovascular drugs : drugs, devices, and other interventions · 2023Review
- Genome-Wide Association Study IdentifiesJournal of clinical oncology : official journal of the American Society of Clinical Oncology · 2023Article
- Smad3 promotes adverse cardiovascular remodeling and dysfunction in doxorubicin-treated hearts.American journal of physiology. Heart and circulatory physiology · 2022Article
- Role of non-cardiomyocytes in anticancer drug-induced cardiotoxicity: A systematic review.iScience · 2022Review
- Cardiac fibrosis in oncologic therapies.Current opinion in physiology · 2022Article
- Cardiac inflammation and fibrosis following chemo/radiation therapy: mechanisms and therapeutic agents.Inflammopharmacology · 2022Review
- Article
- Naringenin Regulates Doxorubicin-Induced Liver Dysfunction: Impact on Oxidative Stress and Inflammation.Plants (Basel, Switzerland) · 2020Article
- Embryonic stem cell-derived cardiomyocytes for the treatment of doxorubicin-induced cardiomyopathy.Stem cell research & therapy · 2018Article
- Anti-hypertensive and cardioprotective effects of a novel apitherapy formulation via upregulation of peroxisome proliferator-activated receptor-α and -γ in spontaneous hypertensive rats.Saudi journal of biological sciences · 2018Article
- VEGF-B gene therapy inhibits doxorubicin-induced cardiotoxicity by endothelial protection.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Elevated ALK4/5 ligands including TGF-β and activins have been linked to cardiovascular remodeling and heart failure. Doxorubicin (Dox) is commonly used as a model of cardiomyopathy, a condition that often precedes cardiovascular remodeling and heart failure. In 7-8-week-old C57Bl/6 male mice treated with Dox we found decreased capillary density, increased levels of ALK4/5 ligand and Smad2/3 transcripts, and increased expression of Smad2/3 transcriptional targets. Human cardiac microvascular endothelial cells (HCMVEC) treated with Dox also showed increased levels of ALK4/5 ligands, Smad2/3 transcriptional targets, a decrease in proliferation and suppression of vascular network formation in a HCMVEC and human cardiac fibroblasts co-culture assay. Our hypothesis is that the deleterious effects of Dox on endothelial cells are mediated in part by the activation of the TGF-β pathway. We used the inhibitor of ALK4/5 kinases SB431542 (SB) in concert with Dox to ascertain the role of TGF-β pathway activation in doxorubicin induced endothelial cell defects. SB prevented the suppression of HCMVEC proliferation in the presence of TGF-β2 and activin A, and alleviated the inhibition of HCMVEC proliferation by Dox. SB also prevented the suppression of vascular network formation in co-cultures of HCMVEC and human cardiac fibroblasts treated with Dox. Our results show that the inhibition of the TGF-β pathway alleviates the detrimental effects of Dox on endothelial cells in vitro.
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.