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Journal Article
International journal of molecular sciences, ISSN 1661-6596, 01/2019, Volume 20, Issue 2, p. 404
Ischemia reperfusion injury (IR injury) associated with ischemic heart disease contributes significantly to morbidity and mortality. O-linked... 
O-GlcNAc | Ischemia-reperfusion injury | Cardioprotection | ATTENUATES OXIDATIVE STRESS | BIOCHEMISTRY & MOLECULAR BIOLOGY | GLCNAC TRANSFERASE | KAPPA-B | BYPASS GRAFT-SURGERY | CHEMISTRY, MULTIDISCIPLINARY | HEXOSAMINE BIOSYNTHESIS | ischemia-reperfusion injury | ONE-YEAR OUTCOMES | BETA-N-ACETYLGLUCOSAMINE | NEONATAL CARDIOMYOCYTES | cardioprotection | ACUTE MYOCARDIAL-INFARCTION | GLUCOSE-INSULIN-POTASSIUM | Myocardial Reperfusion Injury - etiology | Reperfusion Injury - etiology | Mitochondrial Membrane Transport Proteins - metabolism | Reactive Oxygen Species - metabolism | Reperfusion Injury - pathology | Comorbidity | Humans | Cardiotonic Agents - pharmacology | Acetylglucosamine - metabolism | Cardiotonic Agents - therapeutic use | Myocardial Reperfusion Injury - metabolism | Myocardial Reperfusion Injury - pathology | Animals | Reperfusion Injury - prevention & control | Metabolic Networks and Pathways | Protein Processing, Post-Translational | Oxidative Stress - drug effects | Reperfusion Injury - metabolism | Myocardial Reperfusion Injury - prevention & control | Heart | Neonates | Enzymes | Glucosamine | Animal models | Calcium | Cardiac muscle | RNA-mediated interference | Mortality | Thiazoline | Cardiovascular disease | Myocytes | Proteins | Augmentation | Transfection | Reperfusion | Ischemia | Cell cycle | Hypoxia | Attenuation | Ventricle | Injuries
Journal Article
Cardiovascular research, ISSN 0008-6363, 09/2012, Volume 95, Issue 4, pp. 487 - 494
Innate mechanisms of inter-organ protection underlie the phenomenon of remote ischaemic preconditioning (RPc) in which episode(s) of ischaemia and reperfusion... 
Brain | Vagus nerve | Ischaemia/reperfusion injury | Preconditioning | Ischaemia | CARDIAC & CARDIOVASCULAR SYSTEMS | K-ATP CHANNELS | LIMB ISCHEMIA | MYOCARDIAL-ISCHEMIA | BRAIN-STEM | reperfusion injury | LENTIVIRAL VECTORS | CARDIOVASCULAR CONTROL | TRANSGENE EXPRESSION | RAT-HEART | AUTONOMIC NERVOUS-SYSTEM | Myocardial Infarction - genetics | Hindlimb | Receptors, G-Protein-Coupled - metabolism | Brain Stem - metabolism | Vagus Nerve - drug effects | Male | Receptors, Neuropeptide - metabolism | Drosophila Proteins - metabolism | Rhodopsin - metabolism | Recombinant Fusion Proteins - metabolism | Autonomic Fibers, Preganglionic - metabolism | Brain Stem - drug effects | Action Potentials | Myocardial Reperfusion Injury - pathology | Time Factors | Muscarinic Antagonists - pharmacology | Myocardial Infarction - pathology | Neuropeptides - pharmacology | Adenoviridae - genetics | Lentivirus - genetics | Myocardial Infarction - physiopathology | Neural Pathways - physiopathology | Myocardial Reperfusion Injury - genetics | Autonomic Fibers, Preganglionic - drug effects | Disease Models, Animal | Heart - innervation | Muscle, Skeletal - blood supply | Transduction, Genetic | Vagus Nerve - metabolism | Constriction | Rats | Receptors, Neuropeptide - genetics | Atropine - pharmacology | Myocardium - pathology | Myocardial Infarction - metabolism | Rats, Sprague-Dawley | Myocardial Reperfusion Injury - physiopathology | Vagus Nerve - physiopathology | Myocardial Reperfusion Injury - metabolism | Animals | Rhodopsin - genetics | Ischemic Preconditioning, Myocardial - methods | Brain Stem - physiopathology | Myocardial Infarction - prevention & control | Receptors, G-Protein-Coupled - genetics | Drosophila Proteins - genetics | Genetic Vectors | Myocardial Reperfusion Injury - prevention & control | Original
Journal Article
Kidney international, ISSN 0085-2538, 2012, Volume 82, Issue 12, pp. 1271 - 1283
Autophagy is induced in renal tubular cells during acute kidney injury; however, whether this is protective or injurious remains controversial. We address this... 
acute kidney injury | autophagy | Atg7 | cisplatin | ischemia–reperfusion | Ischemia-reperfusion | APOPTOSIS | ACTIVATION | ACUTE-RENAL-FAILURE | PATHOLOGICAL ROLE | ischemia-reperfusion | CISPLATIN NEPHROTOXICITY | CELL-DEATH | PATHOPHYSIOLOGY | UROLOGY & NEPHROLOGY | MICE | BODY FORMATION | SELF-DIGESTION | Microtubule-Associated Proteins - genetics | Blood Urea Nitrogen | JNK Mitogen-Activated Protein Kinases - metabolism | Acute Kidney Injury - genetics | Autophagy - drug effects | Reperfusion Injury - blood | Chloroquine - pharmacology | Time Factors | Reperfusion Injury - chemically induced | Acute Kidney Injury - chemically induced | Microtubule-Associated Proteins - deficiency | Reperfusion Injury - genetics | Cytoprotection | Disease Models, Animal | Kidney Tubules, Proximal - pathology | Reperfusion Injury - pathology | Signal Transduction | Acute Kidney Injury - pathology | Acute Kidney Injury - blood | Mice, Inbred C57BL | Cells, Cultured | Tumor Suppressor Protein p53 - metabolism | Biomarkers - blood | Sirolimus - pharmacology | Acute Kidney Injury - prevention & control | Cisplatin | Mice, Knockout | Autophagy-Related Protein 7 | Animals | Reperfusion Injury - prevention & control | Kidney Tubules, Proximal - metabolism | Creatinine - blood | Mice | Enzyme Activation | Apoptosis | Kidney Tubules, Proximal - drug effects
Journal Article
Journal Article
Cardiovascular research, ISSN 1755-3245, 2019, Volume 115, Issue 7, pp. 1117 - 1130
New therapies are required to reduce myocardial infarct ( MI) size and prevent the onset of heart failure in patients presenting with acute myocardial... 
Monocytes | Dendritic cells | Lymphocytes | Myocardial ischaemia/reperfusion injury | Fibroblasts | Inflammation | Acute myocardial infarction | Macrophages | CARDIAC & CARDIOVASCULAR SYSTEMS | LONG NONCODING RNAS | REGULATES FIBROBLAST PHENOTYPE | CD4(+) T-LYMPHOCYTES | MYOCARDIAL ISCHEMIA/REPERFUSION INJURY | PRECLINICAL ASSESSMENT | ISCHEMIA-REPERFUSION INJURY | INFARCT SIZE | CELLULAR BIOLOGY | CARDIAC MAST-CELLS | Myocardium - immunology | Dendritic Cells - immunology | Humans | Monocytes - metabolism | Monocytes - immunology | Myocardial Infarction - immunology | Heart Failure - prevention & control | Myocardial Infarction - therapy | Myocardial Reperfusion Injury - pathology | Anti-Inflammatory Agents - adverse effects | Lymphocytes - immunology | Myocardial Infarction - pathology | Myocardium - metabolism | Heart Failure - immunology | Inflammation Mediators - metabolism | Mast Cells - metabolism | Anti-Inflammatory Agents - therapeutic use | Dendritic Cells - drug effects | Neutrophils - metabolism | Dendritic Cells - metabolism | Fibroblasts - metabolism | Myocardial Reperfusion Injury - immunology | Inflammation Mediators - immunology | Lymphocytes - metabolism | Mast Cells - immunology | Signal Transduction | Neutrophils - drug effects | Ventricular Function, Left - drug effects | Neutrophils - immunology | Myocardium - pathology | Heart Failure - metabolism | Heart Failure - pathology | Myocardial Infarction - metabolism | Mast Cells - drug effects | Monocytes - drug effects | Cardiovascular Agents - therapeutic use | Myocardial Reperfusion Injury - metabolism | Animals | Fibroblasts - drug effects | Lymphocytes - drug effects | Fibroblasts - immunology | Cardiovascular Agents - adverse effects | Ventricular Remodeling - drug effects | Myocardial Reperfusion Injury - prevention & control | Invited Spotlight Reviews | Myocardial ischaemia | reperfusion injury
Journal Article