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Role of 14-3-3 protein and oxidative stress in diabetic cardiomyopathy
Kenichi Watanabe1, R A Thandavarayan, N Gurusamy
1Department of Clinical Pharmacology, Niigata University of Pharmacy and Applied Life Sciences, 265-1 Higashijima, Akiha-ku, Niigata City, Japan. watanabe@nupals.ac.jp
Insights
Diabetic cardiomyopathy, a heart condition in diabetes patients, is worsened by oxidative stress. Mammalian 14-3-3 proteins are key regulators in its development and progression.
Area of Science:
- Cardiology
- Endocrinology
- Molecular Biology
Background:
- Cardiovascular disease is a major global health concern.
- Diabetes mellitus is a significant risk factor for cardiovascular diseases, leading to diabetic cardiomyopathy independent of other cardiac conditions.
- Oxidative stress, driven by hyperglycemia, exacerbates diabetes and its complications, including cardiac changes.
Purpose of the Study:
- To review the emerging evidence on the role of mammalian 14-3-3 proteins in the pathogenesis of diabetic cardiomyopathy.
- To highlight the involvement of 14-3-3 protein in regulating signaling pathways crucial to cardiovascular complications of diabetes.
Main Methods:
- This review synthesizes current research and emerging evidence.
- Focuses on the molecular mechanisms and signaling pathways involved in diabetic cardiomyopathy.
- Examines the function of 14-3-3 proteins in cellular biochemistry and signal transduction.
Main Results:
- Diabetic cardiomyopathy involves structural changes in the heart and coronary vasculature.
- Myocardial apoptosis, hypertrophy, and fibrosis are proposed mechanisms for cardiac alterations.
- Mammalian 14-3-3 proteins, involved in signal transduction, regulate multiple signaling pathways implicated in diabetic cardiomyopathy.
Conclusions:
- Mammalian 14-3-3 proteins play a critical role in the development and progression of diabetic cardiomyopathy.
- Understanding the role of 14-3-3 proteins may offer new therapeutic targets for managing cardiovascular complications in diabetes.
Abstract:
Cardiovascular disease is a leading cause of death worldwide. Diabetes mellitus is a well-known and important risk factor for cardiovascular diseases. The occurrence of diabetic cardiomyopathy is independent of hypertension, coronary artery disease, or any other known cardiac diseases. There is growing evidence that excess generation of highly reactive free radicals, largely due to hyperglycemia, causes oxidative stress, which further exacerbates the development and progression of diabetes and its complications. Diabetic cardiomyopathy is characterized by morphologic and structural changes in the myocardium and coronary vasculature mediated by the activation of various signaling pathways. Myocardial apoptosis, hypertrophy and fibrosis are the most frequently proposed mechanisms to explain cardiac changes in diabetic cardiomyopathy. Mammalian 14-3-3 proteins are dimeric phosphoserine-binding proteins that participate in signal transduction and regulate several aspects of cellular biochemistry. 14-3-3 protein regulates diabetic cardiomyopathy via multiple signaling pathways. This review focuses on emerging evidence suggesting that 14-3-3 protein plays a key role in the pathogenesis of the cardiovascular complications of diabetes, which underlie the development and progression of diabetic cardiomyopathy.
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