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      Regulated cell death pathways in doxorubicin-induced cardiotoxicity

      review-article
      Author(s): 1 , 1 , 2 , 3 ,
      Publication date (Electronic):
      Journal: Cell Death & Disease
      Publisher: Nature Publishing Group UK
      Keywords: Mechanisms of disease, Cardiomyopathies

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          Abstract

          Doxorubicin is a chemotherapeutic drug used for the treatment of various malignancies; however, patients can experience cardiotoxic effects and this has limited the use of this potent drug. The mechanisms by which doxorubicin kills cardiomyocytes has been elusive and despite extensive research the exact mechanisms remain unknown. This review focuses on recent advances in our understanding of doxorubicin induced regulated cardiomyocyte death pathways including autophagy, ferroptosis, necroptosis, pyroptosis and apoptosis. Understanding the mechanisms by which doxorubicin leads to cardiomyocyte death may help identify novel therapeutic agents and lead to more targeted approaches to cardiotoxicity testing.

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          Most cited references112

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          Ferroptosis: an iron-dependent form of nonapoptotic cell death.

          Scott J. Dixon, Kathryn Lemberg, Michael Lamprecht … (2012)
          Nonapoptotic forms of cell death may facilitate the selective elimination of some tumor cells or be activated in specific pathological states. The oncogenic RAS-selective lethal small molecule erastin triggers a unique iron-dependent form of nonapoptotic cell death that we term ferroptosis. Ferroptosis is dependent upon intracellular iron, but not other metals, and is morphologically, biochemically, and genetically distinct from apoptosis, necrosis, and autophagy. We identify the small molecule ferrostatin-1 as a potent inhibitor of ferroptosis in cancer cells and glutamate-induced cell death in organotypic rat brain slices, suggesting similarities between these two processes. Indeed, erastin, like glutamate, inhibits cystine uptake by the cystine/glutamate antiporter (system x(c)(-)), creating a void in the antioxidant defenses of the cell and ultimately leading to iron-dependent, oxidative death. Thus, activation of ferroptosis results in the nonapoptotic destruction of certain cancer cells, whereas inhibition of this process may protect organisms from neurodegeneration. Copyright © 2012 Elsevier Inc. All rights reserved.
          Article 0 comments Cited 4811 times – based on 0 reviews     Review now
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            Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018

            Lorenzo Galluzzi, Ilio Vitale, Stuart A. Aaronson … (2018)
            Over the past decade, the Nomenclature Committee on Cell Death (NCCD) has formulated guidelines for the definition and interpretation of cell death from morphological, biochemical, and functional perspectives. Since the field continues to expand and novel mechanisms that orchestrate multiple cell death pathways are unveiled, we propose an updated classification of cell death subroutines focusing on mechanistic and essential (as opposed to correlative and dispensable) aspects of the process. As we provide molecularly oriented definitions of terms including intrinsic apoptosis, extrinsic apoptosis, mitochondrial permeability transition (MPT)-driven necrosis, necroptosis, ferroptosis, pyroptosis, parthanatos, entotic cell death, NETotic cell death, lysosome-dependent cell death, autophagy-dependent cell death, immunogenic cell death, cellular senescence, and mitotic catastrophe, we discuss the utility of neologisms that refer to highly specialized instances of these processes. The mission of the NCCD is to provide a widely accepted nomenclature on cell death in support of the continued development of the field.
            Article 0 comments Cited 1927 times – based on 0 reviews     Review now
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              Apoptosis: a review of programmed cell death.

              Susan A. Elmore (2007)
              The process of programmed cell death, or apoptosis, is generally characterized by distinct morphological characteristics and energy-dependent biochemical mechanisms. Apoptosis is considered a vital component of various processes including normal cell turnover, proper development and functioning of the immune system, hormone-dependent atrophy, embryonic development and chemical-induced cell death. Inappropriate apoptosis (either too little or too much) is a factor in many human conditions including neurodegenerative diseases, ischemic damage, autoimmune disorders and many types of cancer. The ability to modulate the life or death of a cell is recognized for its immense therapeutic potential. Therefore, research continues to focus on the elucidation and analysis of the cell cycle machinery and signaling pathways that control cell cycle arrest and apoptosis. To that end, the field of apoptosis research has been moving forward at an alarmingly rapid rate. Although many of the key apoptotic proteins have been identified, the molecular mechanisms of action or inaction of these proteins remain to be elucidated. The goal of this review is to provide a general overview of current knowledge on the process of apoptosis including morphology, biochemistry, the role of apoptosis in health and disease, detection methods, as well as a discussion of potential alternative forms of apoptosis.
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                Author and article information

                Contributors
                Liam R. Brunham:
                ORCID: http://orcid.org/0000-0002-3686-3807
                liam.brunham@ubc.ca
                Journal
                Journal ID (nlm-ta): Cell Death Dis
                Journal ID (iso-abbrev): Cell Death Dis
                Title: Cell Death & Disease
                Publisher: Nature Publishing Group UK (London )
                ISSN (Electronic): 2041-4889
                Publication date (Electronic): 1 April 2021
                Publication date PMC-release: 1 April 2021
                Publication date Collection: April 2021
                Volume: 12
                Issue: 4
                Electronic Location Identifier: 339
                Affiliations
                [1 ]GRID grid.17091.3e, ISNI 0000 0001 2288 9830, Centre for Heart Lung Innovation, Department of Medicine, , University of British Columbia, ; Vancouver, BC Canada
                [2 ]GRID grid.17091.3e, ISNI 0000 0001 2288 9830, Department of Medicine, , University of British Columbia, ; Vancouver, BC Canada
                [3 ]GRID grid.17091.3e, ISNI 0000 0001 2288 9830, Department of Medical Genetics, , University of British Columbia, ; Vancouver, BC Canada
                Author information
                http://orcid.org/0000-0002-3686-3807
                Article
                Publisher ID: 3614
                DOI: 10.1038/s41419-021-03614-x
                PMC ID: 8017015
                PubMed ID: 33795647
                SO-VID: 3e61e816-893e-4f87-8f69-17aa7f46b226
                Copyright © © The Author(s) 2021
                License:

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

                History
                Date received : 3 December 2020
                Date revision received : 10 March 2021
                Date accepted : 11 March 2021
                Funding
                Funded by: Canadian Institutes for Health Research (CIHR) PJT 153118
                Categories
                Subject: Review Article
                Custom metadata
                issue-copyright-statement © The Author(s) 2021

                ScienceOpen disciplines: Cell biology
                Keywords: mechanisms of disease,cardiomyopathies
                Data availability:
                ScienceOpen disciplines: Cell biology
                Keywords: mechanisms of disease, cardiomyopathies

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