Role of Endothelium in Doxorubicin-Induced Cardiomyopathy

Summary: The clinical use of doxorubicin in cancer is limited by cardiotoxic effects that can lead to heart failure. Whereas earlier work focused on the direct impact of doxorubicin on cardiomyocytes, recent studies have turned to the endothelium, because doxorubicin-damaged endothelial cells can tr...

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Main Authors: Albert Z. Luu, BSc, Biswajit Chowdhury, PhD, Mohammed Al-Omran, MD, MSc, Hwee Teoh, PhD, David A. Hess, PhD, Subodh Verma, MD, PhD
Format: Article
Language:English
Published: Elsevier 2018-12-01
Series:JACC: Basic to Translational Science
Online Access:http://www.sciencedirect.com/science/article/pii/S2452302X18301396
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author Albert Z. Luu, BSc
Biswajit Chowdhury, PhD
Mohammed Al-Omran, MD, MSc
Hwee Teoh, PhD
David A. Hess, PhD
Subodh Verma, MD, PhD
author_facet Albert Z. Luu, BSc
Biswajit Chowdhury, PhD
Mohammed Al-Omran, MD, MSc
Hwee Teoh, PhD
David A. Hess, PhD
Subodh Verma, MD, PhD
author_sort Albert Z. Luu, BSc
collection DOAJ
description Summary: The clinical use of doxorubicin in cancer is limited by cardiotoxic effects that can lead to heart failure. Whereas earlier work focused on the direct impact of doxorubicin on cardiomyocytes, recent studies have turned to the endothelium, because doxorubicin-damaged endothelial cells can trigger the development and progression of cardiomyopathy by decreasing the release and activity of key endothelial factors and inducing endothelial cell death. Thus, the endothelium represents a novel target for improving the detection, management, and prevention of doxorubicin-induced cardiomyopathy. Key Words: cardiomyopathy, doxorubicin, endothelium, heart failure
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spelling doaj.art-5ef5f3cb0f8a4f469f825cf9a75ca1d52022-12-22T02:56:04ZengElsevierJACC: Basic to Translational Science2452-302X2018-12-0136861870Role of Endothelium in Doxorubicin-Induced CardiomyopathyAlbert Z. Luu, BSc0Biswajit Chowdhury, PhD1Mohammed Al-Omran, MD, MSc2Hwee Teoh, PhD3David A. Hess, PhD4Subodh Verma, MD, PhD5Division of Cardiac Surgery, Keenan Research Centre for Biomedical Science, St. Michael’s Hospital, Toronto, Ontario, Canada; Department of Pharmacology and Toxicology, University of Toronto, Toronto, Ontario, CanadaDivision of Cardiac Surgery, Keenan Research Centre for Biomedical Science, St. Michael’s Hospital, Toronto, Ontario, CanadaDepartment of Pharmacology and Toxicology, University of Toronto, Toronto, Ontario, Canada; Division of Vascular Surgery, Keenan Research Centre for Biomedical Science, St. Michael’s Hospital, Toronto, Ontario, Canada; Department of Surgery, University of Toronto, Toronto, Ontario, Canada; Department of Surgery, King Saud University, Riyadh, Kingdom of Saudi ArabiaDivision of Cardiac Surgery, Keenan Research Centre for Biomedical Science, St. Michael’s Hospital, Toronto, Ontario, Canada; Division of Endocrinology and Metabolism, Keenan Research Centre for Biomedical Science, St. Michael’s Hospital, Toronto, Ontario, CanadaDepartment of Pharmacology and Toxicology, University of Toronto, Toronto, Ontario, Canada; Division of Vascular Surgery, Keenan Research Centre for Biomedical Science, St. Michael’s Hospital, Toronto, Ontario, Canada; Molecular Medicine Research Laboratories, Krembil Centre for Stem Cell Biology, Robarts Research Institute, London, Ontario, Canada; Department of Physiology and Pharmacology, Schulich School of Medicine and Dentistry, Western University, London, Ontario, Canada; Dr. David A. Hess, Department of Physiology and Pharmacology, Schulich School of Medicine and Dentistry, Western University, 1151 Richmond Street, London, Ontario N6A 5B7, Canada.Division of Cardiac Surgery, Keenan Research Centre for Biomedical Science, St. Michael’s Hospital, Toronto, Ontario, Canada; Department of Pharmacology and Toxicology, University of Toronto, Toronto, Ontario, Canada; Department of Surgery, University of Toronto, Toronto, Ontario, Canada; Address for correspondence: Dr. Subodh Verma, Division of Cardiac Surgery, St. Michael’s Hospital, 8th Floor Bond Wing, 30 Bond Street, Toronto, Ontario M5B 1W8, Canada.Summary: The clinical use of doxorubicin in cancer is limited by cardiotoxic effects that can lead to heart failure. Whereas earlier work focused on the direct impact of doxorubicin on cardiomyocytes, recent studies have turned to the endothelium, because doxorubicin-damaged endothelial cells can trigger the development and progression of cardiomyopathy by decreasing the release and activity of key endothelial factors and inducing endothelial cell death. Thus, the endothelium represents a novel target for improving the detection, management, and prevention of doxorubicin-induced cardiomyopathy. Key Words: cardiomyopathy, doxorubicin, endothelium, heart failurehttp://www.sciencedirect.com/science/article/pii/S2452302X18301396
spellingShingle Albert Z. Luu, BSc
Biswajit Chowdhury, PhD
Mohammed Al-Omran, MD, MSc
Hwee Teoh, PhD
David A. Hess, PhD
Subodh Verma, MD, PhD
Role of Endothelium in Doxorubicin-Induced Cardiomyopathy
JACC: Basic to Translational Science
title Role of Endothelium in Doxorubicin-Induced Cardiomyopathy
title_full Role of Endothelium in Doxorubicin-Induced Cardiomyopathy
title_fullStr Role of Endothelium in Doxorubicin-Induced Cardiomyopathy
title_full_unstemmed Role of Endothelium in Doxorubicin-Induced Cardiomyopathy
title_short Role of Endothelium in Doxorubicin-Induced Cardiomyopathy
title_sort role of endothelium in doxorubicin induced cardiomyopathy
url http://www.sciencedirect.com/science/article/pii/S2452302X18301396
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