ArticleNature communications2021
An antibody against L1 cell adhesion molecule inhibits cardiotoxicity by regulating persistent DNA damage.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
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Who cites it
15 citing papers in PubMed, 24 citations in OpenAlex.
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- Preservation of ALYREF Phase Separation Mitigates Doxorubicin-Induced Cardiomyocyte DNA Damage and Cardiotoxicity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Loss of Predicted Cell Adhesion Molecule MPZL3 Promotes EMT in Ovarian Cancer.Cancer research communications · 2025Article
- A novel carrier-free nanoparticle with stable distinctive three-dimensional structure for tumor-targeted precision chemoimmunotherapy.Journal of nanobiotechnology · 2025Article
- Effects of Proton Therapy on Cardiac Fibrosis, Calcium Homeostasis, and AQP4 Expression in Hypergravity-Exposed Rats.International journal of molecular sciences · 2025Article
- New insights into mitochondrial quality control in anthracycline-induced cardiotoxicity: molecular mechanisms, therapeutic targets, and natural products.International journal of biological sciences · 2025Review
- The Inhibition of Vessel Co-Option as an Emerging Strategy for Cancer Therapy.International journal of molecular sciences · 2024Review
- Sophocarpine alleviates doxorubicin-induced heart injury by suppressing oxidative stress and apoptosis.Scientific reports · 2024Article
- L1 cell adhesion molecule may be a protective molecule for atrial fibrillation in patients with valvular heart disease.Heliyon · 2023Article
- Synthesis of bimetal MOFs for rapid removal of doxorubicin in water by advanced oxidation method.RSC advances · 2022Article
- The Impairment of Cell Metabolism by Cardiovascular Toxicity of Doxorubicin Is Reversed by Bergamot Polyphenolic Fraction Treatment in Endothelial Cells.International journal of molecular sciences · 2022Article
- The p53 Transactivation Domain 1-Dependent Response to Acute DNA Damage in Endothelial Cells Protects against Radiation-Induced Cardiac Injury.Radiation research · 2022Article
- 2-Methoxyestradiol Inhibits Radiation-Induced Skin Injuries.International journal of molecular sciences · 2022Article
- miR-488-3p Protects Cardiomyocytes against Doxorubicin-Induced Cardiotoxicity by Inhibiting CyclinG1.Oxidative medicine and cellular longevity · 2022Article
Corrections and comments
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Authors and funding
17 authors at 6 institutions in 2 countries.
Funding
Abstract
Targeting the molecular pathways underlying the cardiotoxicity associated with thoracic irradiation and doxorubicin (Dox) could reduce the morbidity and mortality associated with these anticancer treatments. Here, we find that vascular endothelial cells (ECs) with persistent DNA damage induced by irradiation and Dox treatment exhibit a fibrotic phenotype (endothelial-mesenchymal transition, EndMT) correlating with the colocalization of L1CAM and persistent DNA damage foci. We demonstrate that treatment with the anti-L1CAM antibody Ab417 decreases L1CAM overexpression and nuclear translocation and persistent DNA damage foci. We show that in whole-heart-irradiated mice, EC-specific p53 deletion increases vascular fibrosis and the colocalization of L1CAM and DNA damage foci, while Ab417 attenuates these effects. We also demonstrate that Ab417 prevents cardiac dysfunction-related decrease in fractional shortening and prolongs survival after whole-heart irradiation or Dox treatment. We show that cardiomyopathy patient-derived cardiovascular ECs with persistent DNA damage show upregulated L1CAM and EndMT, indicating clinical applicability of Ab417. We conclude that controlling vascular DNA damage by inhibiting nuclear L1CAM translocation might effectively prevent anticancer therapy-associated cardiotoxicity.
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