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The Role of Mitochondrial Abnormalities in Diabetic Cardiomyopathy
Siarhei A Dabravolski1, Nikolay K Sadykhov2, Andrey G Kartuesov2
1Department of Clinical Diagnostics, Vitebsk State Academy of Veterinary Medicine [UO VGAVM], 7/11 Dovatora Str., 210026 Vitebsk, Belarus.
Insights
Diabetic cardiomyopathy (DCM) involves heart dysfunction in diabetes. Mitochondrial dysfunction is a key factor, suggesting targeted therapies could be beneficial for managing DCM progression.
Area of Science:
- Cardiology
- Mitochondrial Biology
- Diabetology
Background:
- Diabetic cardiomyopathy (DCM) is characterized by cardiac dysfunction in diabetic patients without other cardiac risk factors.
- Mitochondrial structural and functional abnormalities are central to DCM pathogenesis.
- Current understanding of DCM pathogenesis is incomplete.
Purpose of the Study:
- To review the role of mitochondrial dynamics, biogenesis, mitophagy, calcium metabolism, and bioenergetics in DCM.
- To highlight mitochondria as a therapeutic target for DCM.
Main Methods:
- Literature review focusing on mitochondrial roles in DCM.
- Analysis of studies investigating mitochondrial dynamics, biogenesis, mitophagy, Ca2+ metabolism, and bioenergetics in DCM.
- Synthesis of evidence linking mitochondrial dysfunction to DCM development and progression.
Main Results:
- Mitochondrial dynamics, biogenesis, and mitophagy are significantly altered in DCM.
- Dysregulation of mitochondrial Ca2+ metabolism contributes to DCM.
- Impaired mitochondrial bioenergetics is a hallmark of DCM.
- Mitochondrial dysfunction directly impacts cardiac structure and function in diabetic patients.
Conclusions:
- Mitochondrial dysfunction is a critical determinant in the development and progression of diabetic cardiomyopathy.
- Targeting mitochondrial pathways offers a promising therapeutic strategy to mitigate DCM.
- Further research into mitochondria-targeting therapies is warranted for effective DCM management.
Abstract:
Diabetic cardiomyopathy (DCM) is defined as the presence in diabetic patients of abnormal cardiac structure and performance (such as left ventricular hypertrophy, fibrosis, and arrhythmia) in the absence of other cardiac risk factors (such as hypertension or coronary artery disease). Although the pathogenesis of DCM remains unclear currently, mitochondrial structural and functional dysfunctions are recognised as a central player in the DCM development. In this review, we focus on the role of mitochondrial dynamics, biogenesis and mitophagy, Ca2+ metabolism and bioenergetics in the DCM development and progression. Based on the crucial role of mitochondria in DCM, application of mitochondria-targeting therapies could be effective strategies to slow down the progression of the disease.
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