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Nature, ISSN 0028-0836, 11/2014, Volume 515, Issue 7527, pp. 431 - 435
Journal Article
Nature Medicine, ISSN 1078-8956, 10/2005, Volume 11, Issue 10, pp. 1096 - 1103
Journal Article
Basic Research in Cardiology, ISSN 0300-8428, 7/2018, Volume 113, Issue 4, pp. 1 - 20
Mitochondrial fission and mitophagy are considered key processes involved in the pathogenesis of cardiac microvascular ischemia reperfusion (IR) injury... 
NR4A1 | Medicine & Public Health | FUNDC1 | CK2α | Cardiac microvascular IR injury | Cardiology | Mff | Mitophagy | Mitochondrial fission | MIGRATION | APOPTOSIS | STEM-CELLS | ACTIVATION | CARDIAC & CARDIOVASCULAR SYSTEMS | ACETYLATION | CELL-DEATH | PROTECTS | LIRAGLUTIDE | CK2 alpha | EXENDIN-4 | ENDOTHELIUM | Mitochondrial Dynamics | Microvessels - physiopathology | Dynamins - metabolism | Phosphorylation | Capillary Permeability | Mitochondria, Heart - pathology | Coronary Vessels - physiopathology | Microvessels - pathology | Male | Mitochondrial Proteins - genetics | Casein Kinase II - genetics | Myocardial Reperfusion Injury - enzymology | Vasodilation | Myocardial Reperfusion Injury - pathology | Mitochondrial Proteins - metabolism | Membrane Proteins - metabolism | Microvessels - enzymology | Myocardial Reperfusion Injury - genetics | Disease Models, Animal | Coronary Vessels - pathology | Genetic Predisposition to Disease | Nuclear Receptor Subfamily 4, Group A, Member 1 - genetics | Coronary Vessels - enzymology | Signal Transduction | Membrane Proteins - genetics | Cells, Cultured | Mitochondria, Heart - enzymology | Myocardial Reperfusion Injury - physiopathology | Mice, Knockout | Mitochondrial Degradation | Nuclear Receptor Subfamily 4, Group A, Member 1 - deficiency | Protein Transport | Animals | Nuclear Receptor Subfamily 4, Group A, Member 1 - metabolism | Endothelial Cells - pathology | Endothelial Cells - enzymology | Casein Kinase II - metabolism | Apoptosis | Heart | Translocation | Deactivation | Threonine | Pathogenesis | Homeostasis | Inactivation | Fission | Mitochondria | Reperfusion | Ischemia | Casein | Rodents | Regulatory mechanisms (biology) | Mice | Protein-serine/threonine kinase | Microvasculature | Damage accumulation | Heart diseases | Injuries | Structure-function relationships | Index Medicus
Journal Article
Circulation Research, ISSN 0009-7330, 02/2010, Volume 106, Issue 3, pp. 546 - 550
Journal Article
Basic Research in Cardiology, ISSN 0300-8428, 7/2012, Volume 107, Issue 4, pp. 1 - 13
Accumulating evidence indicatesthat programmed necrosis plays a critical role in cell death during ischemia–reperfusion. Necrostatin-1 (Nec-1), a small... 
Myocardial infarction | Necrostatin-1 | Reperfusion | Medicine & Public Health | Cardiology | Cell death | PERMEABILITY TRANSITION PORE | NADPH OXIDASE | PRESSURE-OVERLOAD | CARDIAC & CARDIOVASCULAR SYSTEMS | HEART-FAILURE | MIXED LINEAGE KINASE | PROGRAMMED NECROSIS | DOMAIN-LIKE | NITRIC-OXIDE | NECROTIC CELL-DEATH | TNF-ALPHA | Receptor-Interacting Protein Serine-Threonine Kinases - metabolism | Phosphorylation | Myocardium - immunology | Reactive Oxygen Species - metabolism | Tumor Necrosis Factor-alpha - genetics | Male | RNA, Messenger - metabolism | Myocardial Infarction - immunology | Myocardial Reperfusion Injury - enzymology | Necrosis | Myocardial Reperfusion Injury - pathology | Time Factors | Myocardial Infarction - pathology | Indoles - pharmacology | Myocardial Infarction - physiopathology | Macrophages - immunology | Neutrophil Infiltration - drug effects | Disease Models, Animal | Myocardial Infarction - enzymology | Myocardial Reperfusion Injury - immunology | Mice, Inbred C57BL | Neutrophils - drug effects | Ventricular Function, Left - drug effects | Neutrophils - immunology | Oxidative Stress - genetics | Stroke Volume - drug effects | Myocardium - pathology | Imidazoles - pharmacology | Myocardial Reperfusion Injury - physiopathology | Myocardium - enzymology | Animals | Macrophages - drug effects | Mice | Myocardial Infarction - prevention & control | Protein Kinase Inhibitors - pharmacology | Oxidative Stress - drug effects | Receptor-Interacting Protein Serine-Threonine Kinases - antagonists & inhibitors | Ventricular Remodeling - drug effects | Myocardial Reperfusion Injury - prevention & control | Apoptosis | Prevention | Messenger RNA | Analysis | Genes | Cardiac patients | Index Medicus
Journal Article
Journal Article
Journal Article
Cardiovascular Research, ISSN 0008-6363, 05/2017, Volume 113, Issue 6, pp. 609 - 619
Aims The preconditioning-like infarct-sparing and anti-inflammatory effects of the peptide hormone relaxin following ischemic injury have been studied in the... 
LV function | eNOS | Ischemia-reperfusion injury | Serelaxin | Caspase-1 | SWINE MODEL | CARDIAC & CARDIOVASCULAR SYSTEMS | HYDROGEN-SULFIDE | PROTECTS | ACUTE HEART-FAILURE | FAMILY PEPTIDES | ROLES | DISEASE | NITRIC-OXIDE | ISCHEMIA-REPERFUSION | RECEPTORS | Inflammasomes - metabolism | Receptors, G-Protein-Coupled - metabolism | Caspase 1 - metabolism | Male | Nitric Oxide Synthase Type III - deficiency | Myocardial Reperfusion Injury - enzymology | Relaxin - pharmacology | Myocardial Reperfusion Injury - pathology | Time Factors | Myocardial Infarction - pathology | Nitrites - blood | Myocardial Infarction - physiopathology | Nitric Oxide Synthase Type III - metabolism | Disease Models, Animal | Myocardial Infarction - enzymology | NLR Family, Pyrin Domain-Containing 3 Protein - metabolism | Mice, Inbred C57BL | Ventricular Function, Left - drug effects | Cells, Cultured | Rats | Myocardium - pathology | Recombinant Proteins - pharmacology | Nitric Oxide Synthase Type III - genetics | Myocardial Reperfusion - methods | Myocardial Reperfusion Injury - physiopathology | Cardiovascular Agents - pharmacology | Mice, Knockout | Myocardial Reperfusion - adverse effects | Myocardium - enzymology | Animals | Signal Transduction - drug effects | Myocardial Infarction - prevention & control | Myocardial Reperfusion Injury - prevention & control | Index Medicus
Journal Article
Journal of Molecular and Cellular Cardiology, ISSN 0022-2828, 2011, Volume 51, Issue 2, pp. 244 - 251
Journal Article