Dysregulation of endothelial cell connexin-43 localisation in response to doxorubicin

Ben Veerman, Samantha-Joe McGivern, Yvonne Dempsie, Patricia E M Martin, Blair Johnston, Susan Currie, Margaret Rose Cunningham

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Introduction: Anthracyclines, such as doxorubicin, remain an important class of chemotherapeutic agent however their efficacy in treating cancer is limited by a cumulative dose-dependent cardiotoxicity. Whilst most studies have focused on cardiomyocyte impairment, circulating doxorubicin has been shown to impact human microvascular responses to doxorubicin in coronary vessels.1 Studies show increased endothelial cell permeability resulting in increased paracellular permeability due to damage to the integrity of cell-cell junctions.2 Strategies to maintain vessel integrity and prevent endothelial cell dysregulation could represent a novel therapeutic opportunity to limit the toxic effects of doxorubicin. The aim of this project was to assess the impact of doxorubicin upon endothelial gap junction proteins, in particular connexin-43 (Cx43).
Original languageEnglish
Article number11
Number of pages1
Issue number1
Publication statusPublished - 5 Apr 2020
Event23rd Annual Meeting Scottish Cardiovascular Forum 2020 - Strathclyde Institute for Pharmacy & Biomedical Sciences, University of Strathclyde, Glasgow, United Kingdom
Duration: 1 Feb 20201 Feb 2020


  • cardiotoxicity
  • connexin-43
  • anthracycline antitumour drugs
  • vascular endothelial cells


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