ArticleJournal of diabetes investigation2021
Effect of adenosine monophosphate-activated protein kinase-p53-Krüppel-like factor 2a pathway in hyperglycemia-induced cardiac remodeling in adult zebrafish.
Article in Journal of diabetes investigation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 12 citations in OpenAlex.
- Molecular remodeling of the myocardium in mice with melanocortin-4 receptor deletion before cardiac function impairment.PloS one · 2026Article
- Zebrafish in Cardiovascular Disease Research: from Model to Application.International journal of biological sciences · 2026Review
- Epilepsy and autophagy modulators: a therapeutic split.Autophagy · 2025Review
- Zebrafish as a Model for Cardiovascular and Metabolic Disease: The Future of Precision Medicine.Biomedicines · 2024Review
- Krüpple-like factors in cardiomyopathy: emerging player and therapeutic opportunities.Frontiers in cardiovascular medicine · 2024Review
- Autophagy and autophagy signaling in Epilepsy: possible role of autophagy activator.Molecular medicine (Cambridge, Mass.) · 2023Review
- Low doses of BPF-induced hypertrophy in cardiomyocytes derived from human embryonic stem cells via disrupting the mitochondrial fission upon the interaction between ERβ and calcineurin A-DRP1 signaling pathway.Cell biology and toxicology · 2022Article
- Zebrafish: A New Promise to Study the Impact of Metabolic Disorders on the Brain.International journal of molecular sciences · 2022Review
- Effect of adenosine monophosphate-activated protein kinase-p53-Krüppel-like factor 2a pathway in hyperglycemia-induced cardiac remodeling in adult zebrafish.Journal of diabetes investigation · 2021Article
- Zebrafish Heart Failure Models.Frontiers in cell and developmental biology · 2021Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
AIMS/
introductionDiabetic cardiomyopathy is a type of myocardial disease. It causes left ventricular hypertrophy, followed by diastolic and systolic dysfunction, eventually leading to congestive heart failure. However, the underlying mechanism still requires further elucidation. MATERIALS AND
methodsA high-glucose zebrafish model was constructed by administering streptozocin intraperitoneally to enhance the development of cardiomyopathy and then treated with adenosine monophosphate-activated protein kinase (AMPK) activator. Cardiac structure and function, and protein and gene expression were then analyzed. Cardiomyocytes (CMs) culture in vitro using lentivirus were used for detection of AMPK, p53 and Krüppel-like factor 2a (klf2a) gene expression.
resultsIn the hyperglycemia group, electrocardiogram findings showed arrhythmia, echocardiography results showed heart enlargement and dysfunction, and many differences, such as increased apoptosis and myocardial fiber loss, were observed. The phospho-AMPK and klf2a expression were downregulated, and p53 expression was upregulated. Activation of phospho-AMPK reduced p53 and increased klf2a expression, alleviated apoptosis in CMs and improved cardiac function in the hyperglycemic zebrafish. In vitro knockdown system of AMPK, p53 and klf2a using lentivirus illustrated an increased p53 expression and decreased klf2a expression in CMs by inhibiting AMPK. Repression of p53 and upregulation of klf2a expression were observed, but no changes in the expression of AMPK and its phosphorylated type.
conclusionsIn the model of streptozocin-induced hyperglycemia zebrafish, the reduction of phosphorylated AMPK increased p53, which led to KLF2a decrease to facilitate apoptosis of CMs, inducing the cardiac remodeling and cardiac dysfunction. These results can be reversed by AMPK activator, which means the AMPK-p53-klf2a pathway might be a potential target for diabetic cardiomyopathy intervention.
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