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Published in: Cardiovascular Toxicology 2/2024

06-02-2024 | Diabetic Cardiomyopathy | Review

Diabetic Cardiomyopathy and Cell Death: Focus on Metal-Mediated Cell Death

Authors: Lu Cai, Yi Tan, Brian Holland, Kupper Wintergerst

Published in: Cardiovascular Toxicology | Issue 2/2024

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Abstract

Cardiac myocyte death is an essential initiator of the pathogenesis and progression of various etiological cardiomyopathies, including diabetic cardiomyopathy (DCM), a disease that has been reported since 1972. Cardiac cell death has been detected in the hearts of patients with diabetes and in animal models, and the role of cell death in the pathogenesis of DCM has been extensively investigated. The first review by the authors, specifically focusing on “Cell death and diabetic cardiomyopathy,” was published in the journal, Cardiovascular Toxicology in 2003. Over the past two decades, studies investigating the role of cardiac cell death in the pathogenesis of DCM have gained significant attention, resulting in the discovery of several new kinds of cell death involving different mechanisms, including apoptosis, necroptosis, pyroptosis, autophagy, ferroptosis, and cuproptosis. After the 20th anniversary of the review published in 2003, we now provide an update with a focus on the potential role of metal-mediated cell death, ferroptosis, and cuproptosis in the development of DCM in compliance with this special issue. The intent of our review is to further stimulate work in the field to advance the body of knowledge and continue to drive efforts to develop more advanced therapeutic approaches to prevent cell death, particularly metal-dependent cell death, and, ultimately, to reduce or prevent the development of DCM.
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Metadata
Title
Diabetic Cardiomyopathy and Cell Death: Focus on Metal-Mediated Cell Death
Authors
Lu Cai
Yi Tan
Brian Holland
Kupper Wintergerst
Publication date
06-02-2024
Publisher
Springer US
Published in
Cardiovascular Toxicology / Issue 2/2024
Print ISSN: 1530-7905
Electronic ISSN: 1559-0259
DOI
https://doi.org/10.1007/s12012-024-09836-7

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