ArticleAmerican journal of physiology. Heart and circulatory physiology2025
Cellular senescence mediates doxorubicin chemotherapy-induced vascular endothelial dysfunction: translational evidence of prevention with senolytic treatment.
Article in American journal of physiology. Heart and circulatory physiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Endothelial Injury as a Potential Contributor to Cardiovascular Toxicity in Hematologic Malignancies.Diseases (Basel, Switzerland) · 2026Review
- Senolytics Reverse PMCardiovascular toxicology · 2026Article
- Mechanisms of Doxorubicin-Induced Cardiac Senescence and Potential Therapeutic Strategies.Biomolecules · 2026Review
- Article
- From signal to significance: characterizing anthracycline-related hypercoagulable adverse events via pharmacovigilance, animal models, and clinical observation.Frontiers in pharmacology · 2026Article
- Article
- Cellular Senescence Mediates Doxorubicin Chemotherapy-Induced Aortic Stiffening: Role of Glycation Stress.Hypertension (Dallas, Tex. : 1979) · 2025Article
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Abstract
Mechanisms underlying doxorubicin (Doxo) chemotherapy-induced vascular endothelial dysfunction are incompletely understood. This study aimed to determine the role of cellular senescence in mediating Doxo-induced vascular endothelial dysfunction and the influence of senolytic therapy as a therapeutic strategy to mitigate endothelial dysfunction with Doxo. Endothelial function [carotid artery endothelium-dependent dilation (EDD) to increasing concentrations of acetylcholine] and associated mechanisms were assessed in young adult p16-3MR mice [which allow for genetic-based clearance of senescent cells with ganciclovir (GCV)] injected with Doxo and subsequently treated with GCV or ABT263 (senolytic). We also assessed the influence of Doxo and ABT263 ex vivo on EDD to increase flow in human arterioles. Lower peak EDD with Doxo (75 ± 3% vs. control, 93 ± 1%;
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