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Diabetic Cardiomyopathy and Cell Death: Focus on Metal-Mediated Cell Death
Lu Cai1,2,3,4, Yi Tan5,6,7, Brian Holland8
1Department of Pediatrics, Pediatric Research Institute, University of Louisville School of Medicine, 570 S. Preston Street, Baxter I, Rm: 304F, Louisville, KY, USA. lu.cai@louisville.edu.
Diabetic cardiomyopathy (DCM) progression involves cardiac myocyte death. This review updates knowledge on cell death mechanisms, focusing on metal-mediated ferroptosis and cuproptosis in DCM pathogenesis.
Area of Science:
- Cardiology
- Cell Biology
- Toxicology
Background:
- Diabetic cardiomyopathy (DCM) is a significant complication of diabetes, characterized by cardiac myocyte death.
- Cardiac cell death has been recognized as a key factor in DCM pathogenesis since 1972.
- Previous reviews have highlighted the role of various cell death pathways in DCM.
Purpose of the Study:
- To provide an updated review on cell death mechanisms in DCM, focusing on metal-mediated cell death.
- To emphasize the potential roles of ferroptosis and cuproptosis in DCM development.
- To stimulate further research into therapeutic strategies targeting cell death in DCM.
Main Methods:
- Literature review of studies investigating cardiac cell death in DCM.
- Analysis of recent findings on apoptosis, necroptosis, pyroptosis, autophagy, ferroptosis, and cuproptosis.
- Focus on metal-dependent cell death mechanisms.
Main Results:
- Over two decades, significant research has identified diverse cell death mechanisms in DCM.
- Emerging evidence points to ferroptosis and cuproptosis as critical contributors to DCM.
- Metal-mediated cell death pathways are increasingly implicated in cardiac pathology.
Conclusions:
- Cardiac myocyte death, particularly metal-dependent forms like ferroptosis and cuproptosis, plays a crucial role in DCM.
- Further investigation into these pathways is essential for developing novel therapeutic interventions.
- Targeting metal-mediated cell death may offer a promising strategy to prevent or treat DCM.
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