ArticleExperimental and therapeutic medicine2022
APPL1 ameliorates myocardial ischemia-reperfusion injury by regulating the AMPK signaling pathway.
Article in Experimental and therapeutic medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- Methyl rosmarinate alleviates myocardial ischemia-reperfusion injury in mice via triggering TGR5/AMPK signaling axis.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Electroacupuncture Pretreatment Alleviates Myocardial Ischemia-Reperfusion Injury by Inhibiting Engulfment by Microglia in the Lateral Hypothalamus.CNS neuroscience & therapeutics · 2025Article
- Protective Effects of Rat Bone Marrow Mesenchymal Stem Cells-Derived Fusogenic Plasma Membrane Vesicles Containing VSVG Protein Mediated Mitochondrial Transfer on Myocardial Injury In Vitro.FASEB bioAdvances · 2025Article
- Protective Role of Oxycodone in Myocardial Oxidative Stress and Mitochondrial Dysfunction Induced by Ischemia-Reperfusion.Journal of biochemical and molecular toxicology · 2025Article
- Review
- METTL14-mediated N6-methyladenosine modification induces the ferroptosis of hypoxia/reoxygenation-induced cardiomyocytes.Journal of cardiothoracic surgery · 2024Article
- Serelaxin Protects H9c2 Cardiac Myoblasts against Hypoxia and Reoxygenation-Induced Damage through Activation of AMP Kinase/Sirtuin1: Further Insight into the Molecular Mechanisms of the Cardioprotection of This Hormone.Antioxidants (Basel, Switzerland) · 2024Article
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4 authors at 3 institutions in 1 country.
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Abstract
Myocardial ischemia-reperfusion injury results in elevated reactive oxygen species (ROS) production and causes oxidative stress damage. Therefore, the current study aimed to investigate whether adaptor protein phosphotyrosine interacting with PH domain and leucine zipper 1 (APPL1) could induce the expression of antioxidant enzymes through AMP-activated protein kinase (AMPK) signaling in order to alleviate the injury caused by ischemia/hypoxia-reperfusion. Following induction of hypoxia-reoxygenation (H/R) injury in H9c2 cells, the liver kinase B1 (LKB1)/AMPK/acetyl-CoA carboxylase α (ACC) signaling pathway was investigated using western blot analysis, along with the detection of superoxide dismutase (SOD)2 and SOD3 expression. Additionally, cell viability was detected using a Cell Counting Kit-8 assay and ROS production was analyzed using ROS staining, whereas the expression levels of inflammatory mediators (TNF-α, monocyte chemoattractant protein 1 and IL-1β), apoptosis mediators [cleaved caspase-3, cleaved poly (ADP-ribose) polymerase and Bcl-2] and nuclear factor erythroid 2-related factor 2 signaling pathway-related proteins were detected via western blot analysis following overexpression of APPL1 alone or in combination with compound C treatment (an AMPK inhibitor). The results indicated that H/R induction upregulated the phosphorylation levels of LKB1, AMPK and ACC, and decreased the expression levels of APPL1 and SOD enzyme activities. APPL1 overexpression increased the phosphorylation levels of LKB1, AMPK and ACC, SOD enzyme activity and cell viability whereas the expression levels of proinflammatory mediators and proapoptotic mediators, and the levels of ROS production were markedly decreased when compared with H/R group with empty plasmid transfection. APPL overexpression-mediated effects were significantly abrogated by compound C. Taken together, the data indicated that APPL1 inhibited ROS production and H/R-induced myocardial injury via the AMPK signaling pathway. Therefore, APPL1 may serve as a potential therapeutic target for myocardial H/R injury.
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