Impairment of Endothelial-Myocardial Interaction Increases the Susceptibility of Cardiomyocytes to Ischemia/Reperfusion Injury

Keyphrases

• Ischemia-reperfusion Injury 100%
• Cardiomyocytes 100%
• Endothelial Cells 100%
• Hyperglycemia 80%
• Endothelial Nitric Oxide Synthase (eNOS) 60%
• Nitric Oxide Production 60%
• Reperfusion 40%
• Triton X-100 (TX-100) 40%
• Lactate Dehydrogenase Activity 40%
• Phosphorylation 20%
• Left Ventricular Function 20%
• Cardioprotection 20%
• Left Ventricular Systolic Function 20%
• Ischemia 20%
• Overexpression 20%
• Hypoxia 20%
• Oxidative Stress 20%
• Cell-derived 20%
• Langendorff 20%
• Rate-limiting Enzyme 20%
• Tetrahydrobiopterin 20%
• Myocardial Injury 20%
• Genetic Approach 20%
• Deoxygenation 20%
• Endothelial Dysfunction 20%
• Mouse Heart 20%
• Myocardial Ischemia-reperfusion Injury 20%
• Pharmacological Approaches 20%
• Hypoxia-reoxygenation 20%
• Dihydrobiopterin 20%
• Incompetence 20%
• GTP Cyclohydrolase I 20%
• Hypoxia Injury 20%
• Sepiapterin 20%

Biochemistry, Genetics and Molecular Biology

• Reperfusion 100%
• Cardiac Muscle Cell 100%
• Hyperglycemia 66%
• Nitric Oxide 50%
• Nitric Oxide Synthase 50%
• Reoxygenation 50%
• Lactate Dehydrogenase 33%
• Enzyme 16%
• Precursor 16%
• Mouse 16%
• Oxidative Stress 16%
• Tetrahydrobiopterin 16%
• Anabolism 16%
• Genetic Approach 16%
• GTP Cyclohydrolase I 16%

Pharmacology, Toxicology and Pharmaceutical Science

• Dihydrobiopterin 25%