ArticleAnnals of translational medicine2022
Targeted activation of ERK1/2 reduces ischemia and reperfusion injury in hyperglycemic myocardium by improving mitochondrial function.
Article in Annals of translational medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 15 citations in OpenAlex.
- Article
- Chronic therapy with α1A-adrenergic agonist reverses RV failure and mitochondrial dysfunction.bioRxiv : the preprint server for biology · 2026Article
- PANoptosis in diabetic retinopathy: immunological insights into mechanisms and translational therapies.Frontiers in immunology · 2026Review
- Exploration of the Potential Bioactive Compounds and Functional Mechanism of Chaihu Sanshen Capsule in Ameliorating Myocardial Ischaemia-Reperfusion Injury: A Serum Pharmaco-Chemistry With Network Pharmacology Analysis.Journal of cellular and molecular medicine · 2025Article
- Effects of High Glucose on Simulated Ischemia/Reperfusion Injury in Isolated Cardiomyocytes.International journal of molecular sciences · 2025Article
- Piezo1 deletion mitigates diabetic cardiomyopathy by maintaining mitochondrial dynamics via ERK/Drp1 pathway.Cardiovascular diabetology · 2025Article
- Identification of Disease-Relevant, Sex-Based Proteomic Differences in iPSC-Derived Vascular Smooth Muscle Cells.International journal of molecular sciences · 2024Article
- Ginsenoside Rg1 treats chronic heart failure by downregulating ERK1/2 protein phosphorylation.In vitro cellular & developmental biology. Animal · 2024Article
- Identification of mitochondria-related gene biomarkers associated with immune infiltration in acute myocardial infarction.iScience · 2024Article
- Article
- Expression Pattern and Molecular Mechanism of Oxidative Stress-Related Genes in Myocardial Ischemia-Reperfusion Injury.Journal of cardiovascular development and disease · 2023Article
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
Background: Diabetes can increase the risk of coronary heart disease, and also increase the mortality rate of coronary heart disease in diabetic patients. Although reperfusion therapy can preserve the viable myocardium, fatal reperfusion injury can also occur. Studies have shown that diabetes can aggravate myocardial ischemia-reperfusion injury, ERK1/2 can reduce myocardial ischemia-reperfusion injury, but its mechanism in hyperglycemic myocardial ischemia-reperfusion injury is unclear. This study sought to explore the mechanism of extracellular signal-regulated kinase 1/2 (ERK1/2) in hyperglycemic myocardial ischemia reperfusion (I/R) injury. Methods: H9C2 cardiomyocytes were treated with high-glucose (HG) medium plus I/R stimulation to establish a hyperglycemia I/R model Results: The HG I/R injury intervention caused an increase in the ratio of apoptotic cardiomyocytes (P<0.05), but the phosphorylation level of the ERK1/2 protein did not increase further. Administering LM22B-10 or transfecting the Conclusions: Targeting the activation of ERK1/2 protein phosphorylation reduced mitochondrial fission, increased membrane potential and mitochondrial function, reduced oxidative stress and myocardial cell apoptosis, and alleviated hyperglycemia myocardial I/R injury.
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