Mitochondrial quality control mechanisms as therapeutic targets in doxorubicin-induced cardiotoxicity |
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| Institution: | 1. Department of Cardiology and Shanghai Institute of Cardiovascular Disease, Zhongshan Hospital, Fudan University, Shanghai 200032, China;1. Department of Biochemistry, University of São Paulo, São Paulo, Brazil;1. Universidad Nacional de Colombia-Sede Bogotá, Departamento de Farmacia, Mimetismo molecular de los Agentes infecciosos, Bogotá, DC, Colombia;2. Centre National de la Recherche scientifique–Université de Strasbourg, Biotechnology and Cell Signalling Unit, Neuroimmunology and Peptide Therapeutics Team, Strasbourg Drug Discovery and Development Institute, Strasbourg, France;3. University of Strasbourg Institute for Advanced Study, Strasbourg, France;4. Fédération Hospitalo-Universitaire OMICARE, Fédération de Médecine Translationnelle de Strasbourg, University of Strasbourg, Strasbourg, France;1. Center for Dementia Research, Nathan Kline Institute, Orangeburg, NY 10962, USA;2. Department of Psychiatry, New York University Grossman School of Medicine, New York, NY 10016, USA;3. Department of Neuroscience and Physiology, New York University Grossman School of Medicine, New York, NY 10016, USA;4. NYU Neuroscience Institute, New York University Grossman School of Medicine, New York, NY 10016, USA;5. Program in Chemical Biology, Sloan Kettering Institute, New York, NY 10065, USA;6. Breast Cancer Medicine Service, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA;1. Department of Biochemistry and Molecular Biology, Institute for Medical Research Israel-Canada, Hebrew University, Hadassah Medical School, Jerusalem 91120, Israel |
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| Abstract: | Doxorubicin (DOX) is a chemotherapeutic drug that is utilized for solid tumors and hematologic malignancies, but its clinical application is hampered by life-threatening cardiotoxicity including cardiac dilation and heart failure. Mitochondrial quality control processes, including mitochondrial proteostasis, mitophagy, and mitochondrial dynamics and biogenesis, serve to maintain mitochondrial homeostasis in the cardiovascular system. Importantly, recent advances have unveiled a major role for defective mitochondrial quality control in the etiology of DOX cardiomyopathy. Moreover, specific interventions targeting these quality control mechanisms to preserve mitochondrial function have emerged as potential therapeutic strategies to attenuate DOX cardiotoxicity. However, clinical translation is challenging because of obscure mechanisms of action and potential adverse effects. The purpose of this review is to provide new insights regarding the role of mitochondrial quality control in the pathogenesis of DOX cardiotoxicity, and to explore promising therapeutic approaches targeting these mechanisms to aid clinical management. |
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