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      Role of Endothelium in Doxorubicin-Induced Cardiomyopathy

      review-article
      Author(s): , BSc a , b , , PhD a , , MD, MSc b , c , d , e , , PhD a , f , , PhD b , c , g , h , ∗∗ , , MD, PhD a , b , d , ∗
      Publication date (Electronic):
      Journal: JACC: Basic to Translational Science
      Publisher: Elsevier
      Keywords: cardiomyopathy, doxorubicin, endothelium, heart failure, AKT, protein kinase B, Bcl-2, B-cell lymphoma-2, DNA, deoxyribonucleic acid, ERK1/2, extracellular signal-regulated kinase 1/2, ET, endothelin, LV, left ventricular, MRP, multidrug resistance protein, NADPH, nicotinamide adenine dinucleotide phosphate, NO, nitric oxide, NOS, nitric oxide synthase, NRG-1, neuregulin-1, PGI2, prostaglandin I2, PI3K, phosphoinositide 3-kinase, RNS, reactive nitrogen species, ROS, reactive oxygen species, ZO, zona occludens

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          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.

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          Phenotypic heterogeneity of the endothelium: II. Representative vascular beds.

          William C. Aird (2007)
          Endothelial cells, which form the inner cellular lining of blood vessels and lymphatics, display remarkable heterogeneity in structure and function. This is the second of a 2-part review on the phenotypic heterogeneity of blood vessel endothelial cells. The first part discusses the scope, the underlying mechanisms, and the diagnostic and therapeutic implications of phenotypic heterogeneity. Here, these principles are applied to an understanding of organ-specific phenotypes in representative vascular beds including arteries and veins, heart, lung, liver, and kidney. The goal is to underscore the importance of site-specific properties of the endothelium in mediating homeostasis and focal vascular pathology, while at the same time emphasizing the value of approaching the endothelium as an integrated system.
          Article 0 comments Cited 329 times – based on 0 reviews     Review now
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            Doxorubicin Cardiomyopathy

            Kanu Chatterjee, Jianqing Zhang, Norman Honbo … (2010)
            Established doxorubicin cardiomyopathy is a lethal disease. When congestive heart failure develops, mortality is approximately 50%. Extensive research has been done to understand the mechanism and pathophysiology of doxorubicin cardiomyopathy, and considerable knowledge and experience has been gained. Unfortunately, no effective treatment for established doxorubicin cardiomyopathy is presently available. Extensive research has been done and is being done to discover preventive treatments. However an effective and clinically applicable preventive treatment is yet to be discovered.
            Article 0 comments Cited 327 times – based on 0 reviews     Review now
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              An APAF-1.cytochrome c multimeric complex is a functional apoptosome that activates procaspase-9.

              H. Zou, Y. Li, X. Liu … (1999)
              We report here the reconstitution of the de novo procaspase-9 activation pathway using highly purified cytochrome c, recombinant APAF-1, and recombinant procaspase-9. APAF-1 binds and hydrolyzes ATP or dATP to ADP or dADP, respectively. The hydrolysis of ATP/dATP and the binding of cytochrome c promote APAF-1 oligomerization, forming a large multimeric APAF-1.cytochrome c complex. Such a complex can be isolated using gel filtration chromatography and is by itself sufficient to recruit and activate procaspase-9. The stoichiometric ratio of procaspase-9 to APAF-1 is approximately 1 to 1 in the complex. Once activated, caspase-9 disassociates from the complex and becomes available to cleave and activate downstream caspases such as caspase-3.
              Article 0 comments Cited 213 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                David A. Hess
                Subodh Verma
                Journal
                Journal ID (nlm-ta): JACC Basic Transl Sci
                Journal ID (iso-abbrev): JACC Basic Transl Sci
                Title: JACC: Basic to Translational Science
                Publisher: Elsevier
                ISSN (Electronic): 2452-302X
                Publication date PMC-release: 31 December 2018
                Publication date Collection: December 2018
                Publication date (Electronic): 31 December 2018
                Volume: 3
                Issue: 6
                Pages: 861-870
                Affiliations
                [a ]Division of Cardiac Surgery, Keenan Research Centre for Biomedical Science, St. Michael’s Hospital, Toronto, Ontario, Canada
                [b ]Department of Pharmacology and Toxicology, University of Toronto, Toronto, Ontario, Canada
                [c ]Division of Vascular Surgery, Keenan Research Centre for Biomedical Science, St. Michael’s Hospital, Toronto, Ontario, Canada
                [d ]Department of Surgery, University of Toronto, Toronto, Ontario, Canada
                [e ]Department of Surgery, King Saud University, Riyadh, Kingdom of Saudi Arabia
                [f ]Division of Endocrinology and Metabolism, Keenan Research Centre for Biomedical Science, St. Michael’s Hospital, Toronto, Ontario, Canada
                [g ]Molecular Medicine Research Laboratories, Krembil Centre for Stem Cell Biology, Robarts Research Institute, London, Ontario, Canada
                [h ]Department of Physiology and Pharmacology, Schulich School of Medicine and Dentistry, Western University, London, Ontario, Canada
                Author notes
                [∗ ] 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. vermasu@ 123456smh.ca
                [∗∗ ]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. dhess@ 123456robarts.ca
                Article
                Publisher ID: S2452-302X(18)30139-6
                DOI: 10.1016/j.jacbts.2018.06.005
                PMC ID: 6314956
                PubMed ID: 30623145
                SO-VID: 36c00ee3-c0b1-4a44-a06e-584b7ecbda89
                Copyright © © 2018 The Authors
                License:

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                Date received : 5 June 2018
                Date accepted : 19 June 2018
                Categories
                Subject: STATE-OF-THE-ART REVIEW

                Keywords: cardiomyopathy,doxorubicin,endothelium,heart failure,akt, protein kinase b,bcl-2, b-cell lymphoma-2,dna, deoxyribonucleic acid,erk1/2, extracellular signal-regulated kinase 1/2,et, endothelin,lv, left ventricular,mrp, multidrug resistance protein,nadph, nicotinamide adenine dinucleotide phosphate,no, nitric oxide,nos, nitric oxide synthase,nrg-1, neuregulin-1,pgi2, prostaglandin i2,pi3k, phosphoinositide 3-kinase,rns, reactive nitrogen species,ros, reactive oxygen species,zo, zona occludens
                Data availability:
                Keywords: cardiomyopathy, doxorubicin, endothelium, heart failure, akt, protein kinase b, bcl-2, b-cell lymphoma-2, dna, deoxyribonucleic acid, erk1/2, extracellular signal-regulated kinase 1/2, et, endothelin, lv, left ventricular, mrp, multidrug resistance protein, nadph, nicotinamide adenine dinucleotide phosphate, no, nitric oxide, nos, nitric oxide synthase, nrg-1, neuregulin-1, pgi2, prostaglandin i2, pi3k, phosphoinositide 3-kinase, rns, reactive nitrogen species, ros, reactive oxygen species, zo, zona occludens

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