ArticleArchives of medical science : AMS2015
Apelin-13 protects the heart against ischemia-reperfusion injury through the RISK-GSK-3β-mPTP pathway.
Article in Archives of medical science : AMS, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 47 citations in OpenAlex.
- Chronic quercetin supplementation modulates cardiac function and signaling pathways in aged male Wistar rat hearts subjected to ischemia-reperfusion.Frontiers in cardiovascular medicine · 2026Article
- Emerging therapy strategies for energy metabolism in acute myocardial infarction.Journal of translational medicine · 2025Review
- The Impact of the Apelinergic System on the Cardiovascular System.International journal of molecular sciences · 2025Review
- Neuroprotective effect of apelin-13 and other apelin forms-a review.Pharmacological reports : PR · 2024Review
- GIP attenuates neuronal oxidative stress by regulating glucose uptake in spinal cord injury of rat.CNS neuroscience & therapeutics · 2024Article
- Mechanistic Implications of GSK and CREB Crosstalk in Ischemia Injury.Neurotoxicity research · 2023Review
- Apelin-13 protects against cisplatin-induced ototoxicity by inhibiting apoptosis and regulating STAT1 and STAT3.Archives of toxicology · 2023Article
- Neuroprotective Roles of Apelin-13 in Neurological Diseases.Neurochemical research · 2023Review
- APJ as Promising Therapeutic Target of Peptide Analogues in Myocardial Infarction- and Hypertension-Induced Heart Failure.Pharmaceutics · 2023Review
- Natural compounds regulate the PI3K/Akt/GSK3β pathway in myocardial ischemia-reperfusion injury.Cell cycle (Georgetown, Tex.) · 2023Article
- Apelin Is a Prototype of Novel Drugs for the Treatment of Acute Myocardial Infarction and Adverse Myocardial Remodeling.Pharmaceutics · 2023Review
- Morphine Prevents Ischemia/Reperfusion-Induced Myocardial Mitochondrial Damage by Activating δ-opioid Receptor/EGFR/ROS Pathway.Cardiovascular drugs and therapy · 2022Article
- A network map of apelin-mediated signaling.Journal of cell communication and signaling · 2022Article
- Apelin-13 inhibits apoptosis and excessive autophagy in cerebral ischemia/reperfusion injury.Neural regeneration research · 2021Article
- Review
- Salidroside Ameliorates Mitochondria-Dependent Neuronal Apoptosis after Spinal Cord Ischemia-Reperfusion Injury Partially through Inhibiting Oxidative Stress and Promoting Mitophagy.Oxidative medicine and cellular longevity · 2020Article
- Correlation between sperm mitochondrial ND5 and ND6 gene variations and total fertilisation failure.Archives of medical science : AMS · 2020Article
- International Union of Basic and Clinical Pharmacology. CVII. Structure and Pharmacology of the Apelin Receptor with a Recommendation that Elabela/Toddler Is a Second Endogenous Peptide Ligand.Pharmacological reviews · 2019Review
- 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
- Inducible and endothelial nitric oxide synthase distribution and expression with hind limb per-conditioning of the rat kidney.Archives of medical science : AMS · 2019Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionApelin plays an important role in the protection against myocardial ischemia-reperfusion (I/R) injury, while the mechanism still remains unclear. In the current study, we aimed to evaluate the protective effect of apelin-13, and the main mechanism. MATERIAL AND
methodsThe in vivo I/R injury model (Sprague-Dawley rat) was established, then infarct size, expression levels of phospho-protein kinase B (p-Akt), phospho-extracellular signal-regulated kinase (p-ERK) and phospho-glycogen synthase kinase-3β (p-GSK-3β) were measured. The fluorescence intensity of tetramethylrhodamine ethyl ester perchlorate (TMRE) of the isolated myocardial cells was determined to evaluate the opening of the mitochondrial permeability transition pore (mPTP) caused by oxidant stress and hypoxia/reoxygenation.
resultsFor the established I/R injury model, apelin-13 and SB216763 (GSK-3β inhibitor) significantly reduced the infarct size (p < 0.05), which could be abolished by LY294002 (PI3K inhibitor), PD98059 (MEK inhibitor) and atractyloside (mPTP accelerator). The enhanced expression levels of p-Akt, p-ERK and p-GSK-3β caused by apelin-13 (p < 0.05) could be counteracted by LY294002 and PD98059. The reduced fluorescence intensity of TMRE in the H2O2/apelin-13 and H2O2/SB216763 treated groups was significantly lower (p < 0.05), indicating that apelin-13 and SB216763 could reduce the decline in mitochondrial membrane potential caused by oxidant stress, and the fluorescence intensity in the hypoxia/reoxygenation + apelin-13 group was significantly lower (p < 0.05), which suggested that apelin-13 could inhibit the mitochondrial membrane potential changes induced by hypoxia/reoxygenation.
conclusionsThe protective mechanism of apelin-13 might be that inactivation of GSK-3β could inhibit the opening of mPTP by activating PI3K/Akt and ERK1/2 involved in the reperfusion injury salvage kinase (RISK) pathway.
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