Investigation of Cardiac Hypertrophy in Different Animal Models of Diabetes: A Narrative Review
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F Ramezani-Aliakbari , D Shakibaei , SE Khoshnam , Kh Ramezani-Aliakbari |
Department of Pathobiology, Faculty of Veterinary Science, Bu-Ali Sina University, Hamadan, I.R. Iran. , kh.ramezanialiakbari@basu.ac.ir |
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Abstract: (440 Views) |
According to the World Health Organization (WHO) reports, cardiovascular diseases are the leading causes of death worldwide. Cardiac hypertrophy is associated with underlying disorders such as diabetes and hypertension. Cardiac hypertrophy is characterized by an increase in the size of cardiomyocytes, high cardiac expression of fetal genes, excessive protein synthesis, and interstitial fibrosis, leading to contractile dysfunction and heart failure. Various mediators, such as cytokines, adhesion molecules, cytoskeleton proteins, adrenergic system activity, natriuretic peptides, changes in energy metabolism, and oxidative stress, are involved in the induction of cardiac hypertrophy. Regarding the clinical importance of cardiac hypertrophy, the development of animal models may culminate in progress in finding novel therapeutic methods for improving heart failure and reducing cardiac disorders. Diabetic models with cardiac hypertrophy can be induced by high-fat/high-sugar diets, toxins such as streptozotocin, and genetic manipulation through induced mutation of leptin or leptin receptor genes. Diet-induced and mutation-induced diabetic models are more likely to show cardiac hypertrophy, while diet-induced diabetic models are particularly suitable for research on lifestyle-related diabetes in humans. Nevertheless, the findings obtained from animal models evaluating diabetic-induced hypertrophy in humans have limitations that require further research to develop new animal models. |
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Keywords: Animal models, Cardiac hypertrophy, Cardiovascular disease, Diabetes |
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Full-Text [PDF 1348 kb]
(171 Downloads)
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Type of Study: Review |
Subject:
Cardiology Received: 2023/10/9 | Accepted: 2024/03/16 | Published: 2023/09/1
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