ArticleInternational journal of cardiology2016
Apelin-13 infusion salvages the peri-infarct region to preserve cardiac function after severe myocardial injury.
Article in International journal of cardiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Early Administration of Apelin Could Prevent Heart Failure Following Myocardial Injury; A Systematic Review and Meta-Analysis.Archives of academic emergency medicine · 2025Review
- Myocardial Viability Imaging using Manganese-Enhanced MRI in the First Hours after Myocardial Infarction.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2021Article
- An injectable thermosensitive hydrogel for sustained release of apelin-13 to enhance flap survival in rat random skin flap.Journal of materials science. Materials in medicine · 2019Article
- Apelinergic System Structure and Function.Comprehensive Physiology · 2017Review
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9 authors.
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Abstract
backgroundApelin-13 (A13) regulates cardiac homeostasis. However, the effects and mechanism of A13 infusion after an acute myocardial injury (AMI) have not been elucidated. This study assesses the restorative effects and mechanism of A13 on the peri-infarct region in murine AMI model.
methods51 FVB/N mice (12weeks, 30g) underwent AMI. A week following injury, continuous micro-pump infusion of A13 (0.5μg/g/day) and saline was initiated for 4-week duration. Dual contrast MRI was conducted on weeks 1, 2, 3, and 5, consisting of delayed-enhanced and manganese-enhanced MRI. Four mice in each group were followed for an extended period of 4weeks without further infusion and underwent MRI scans on weeks 7 and 9.
resultsA13 infusion demonstrated preserved LVEF compared to saline from weeks 1 to 4 (21.9±3.2% to 23.1±1.7%* vs. 23.5±1.7% to 16.9±2.8%, *p=0.02), which persisted up to 9weeks post-MI (+1.4%* vs. -9.4%, *p=0.03). Mechanistically, dual contrast MRI demonstrated significant decrease in the peri-infarct and scar % volume in A13 group from weeks 1 to 4 (15.1 to 7.4% and 34.3 to 25.1%, p=0.02, respectively). This was corroborated by significant increase in 5-ethynyl-2'-deoxyuridine (EdU(+)) cells by A13 vs. saline groups in the peri-infarct region (16.5±3.1% vs. 8.1±1.6%; p=0.04), suggesting active cell mitosis. Finally, significantly enhanced mobilization of CD34(+) cells in the peripheral blood and up-regulation of APJ, fibrotic, and apoptotic genes in the peri-infarct region were found.
conclusionsA13 preserves cardiac performance by salvaging the peri-infarct region and may contribute to permanent restoration of the severely injured myocardium.
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