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Journal of Clinical Investigation, ISSN 0021-9738, 02/2015, Volume 125, Issue 2, pp. 715 - 726
Journal Article
Kidney International, ISSN 0085-2538, 06/2013, Volume 83, Issue 6, pp. 1087 - 1098
Netrin-1 regulates inflammation but the mechanism by which this occurs is unknown. Here we explore the role of netrin-1 in regulating the production of the... 
PGE2 | cyclooxygenase | inflammation | netrin-1 | Cyclooxygenase | Inflammation | Netrin-1 | CELLS | ISCHEMIA/REPERFUSION INJURY | IFN-GAMMA PRODUCTION | COX-2 | REPERFUSION INJURY | PULMONARY INFLAMMATION | RECEPTOR | ACUTE-RENAL-FAILURE | HYPOXIA | DISEASE | UROLOGY & NEPHROLOGY | Inflammation - pathology | Homeodomain Proteins - metabolism | Kidney - enzymology | Kidney - immunology | NF-kappa B - metabolism | Acute Kidney Injury - genetics | Nerve Growth Factors - pharmacology | Time Factors | Cyclooxygenase 2 - genetics | Inflammation Mediators - metabolism | Acute Kidney Injury - immunology | Reperfusion Injury - genetics | Macrophages - immunology | Neutrophil Infiltration - drug effects | Disease Models, Animal | Cell Line | Kidney - drug effects | Cytokines - metabolism | Neutrophils - enzymology | Reperfusion Injury - pathology | Acute Kidney Injury - pathology | Anti-Inflammatory Agents - pharmacology | Reperfusion Injury - enzymology | Down-Regulation | Neutrophils - drug effects | Neutrophils - immunology | Inflammation - immunology | Recombinant Proteins - pharmacology | Acute Kidney Injury - enzymology | Acute Kidney Injury - prevention & control | Homeodomain Proteins - genetics | Macrophages - enzymology | Mice, Knockout | Dinoprostone - metabolism | Animals | Reperfusion Injury - prevention & control | Reperfusion Injury - immunology | Cyclooxygenase 2 - metabolism | Inflammation - genetics | Tumor Suppressor Proteins - pharmacology | Macrophages - drug effects | Inflammation - prevention & control | Mice | Macrophage Activation - drug effects | Inflammation - enzymology | Index Medicus | Animal models
Journal Article
Science Translational Medicine, ISSN 1946-6234, 12/2015, Volume 7, Issue 318, p. 318ra200
Autoantibodies to components of apoptotic cells, such as anti-perlecan antibodies, contribute to rejection in organ transplant recipients. However, mechanisms... 
SOLID-ORGAN TRANSPLANTATION | MEDICINE, RESEARCH & EXPERIMENTAL | ACUTE KIDNEY INJURY | SYSTEMIC-LUPUS-ERYTHEMATOSUS | CORONARY-ARTERY DISEASE | EXTRACELLULAR VESICLES | ANTIVIMENTIN ANTIBODIES | PERLECAN FRAGMENT LG3 | NON-HLA ANTIBODIES | MESENCHYMAL STEM-CELLS | CHRONIC ALLOGRAFT NEPHROPATHY | CELL BIOLOGY | Cell-Derived Microparticles - enzymology | Humans | Muscle, Smooth, Vascular - immunology | Immunity, Humoral | Ischemia - immunology | Time Factors | Peptide Fragments - immunology | Exosomes - immunology | Acute Kidney Injury - immunology | Proteomics - methods | Graft Rejection - pathology | Proteasome Endopeptidase Complex - immunology | Ischemia - pathology | Aorta - transplantation | Disease Models, Animal | Biomarkers - metabolism | Acute Kidney Injury - pathology | Myocytes, Smooth Muscle - enzymology | Rats | Aorta - immunology | Acute Kidney Injury - enzymology | Aorta - pathology | Human Umbilical Vein Endothelial Cells - enzymology | Exosomes - enzymology | Human Umbilical Vein Endothelial Cells - pathology | Mice, Inbred BALB C | Graft Rejection - immunology | Proteasome Endopeptidase Complex - metabolism | Muscle, Smooth, Vascular - enzymology | Ischemia - enzymology | Myocytes, Smooth Muscle - pathology | Human Umbilical Vein Endothelial Cells - immunology | Exosomes - pathology | Autoantibodies - biosynthesis | Allografts | Cell-Derived Microparticles - pathology | Kidney Tubules, Proximal - enzymology | Aorta - enzymology | Graft Rejection - enzymology | Kidney Tubules, Proximal - immunology | Kidney Tubules, Proximal - pathology | Peptide Fragments - metabolism | Mice, Inbred C57BL | Cells, Cultured | Heparan Sulfate Proteoglycans - immunology | Autoantibodies - immunology | Muscle, Smooth, Vascular - pathology | Animals | Apoptosis - immunology | Cell-Derived Microparticles - immunology | Heparan Sulfate Proteoglycans - metabolism | Myocytes, Smooth Muscle - immunology
Journal Article
American Journal of Physiology - Renal Physiology, ISSN 0363-6127, 04/2014, Volume 306, Issue 7, pp. F734 - F743
Acute kidney injury (AKI) is a complication of sepsis and leads to a high mortality rate. Human and animal studies suggest that mitochondrial dysfunction plays... 
Mitochondrial antioxidant | Oxidative stress | Sepsis | Mitochondria | Kidney | ACUTE KIDNEY INJURY | PHYSIOLOGY | PERITUBULAR CAPILLARY DYSFUNCTION | MECHANISM | mitochondria | PGC-1-ALPHA | MICROCIRCULATION | kidney | THERAPY | BIOGENESIS | SEPTIC SHOCK | UROLOGY & NEPHROLOGY | mitochondrial antioxidant | GENERATION | sepsis | oxidative stress | Mitochondria - enzymology | Electron Transport Complex III - metabolism | Kidney - blood supply | Kidney - pathology | Kidney - enzymology | Male | Electron Transport Complex I - metabolism | Microcirculation - drug effects | Electron Transport Complex IV - metabolism | Sepsis - drug therapy | Sepsis - pathology | Piperidines - pharmacology | Time Factors | Adenosine Triphosphate - metabolism | Cell Respiration - drug effects | Organophosphorus Compounds - pharmacology | Body Temperature Regulation - drug effects | Renal Circulation - drug effects | Superoxide Dismutase - metabolism | Disease Models, Animal | Kidney - drug effects | Acute Kidney Injury - pathology | Mice, Inbred C57BL | Antioxidants - pharmacology | Mitochondria - drug effects | Mitochondria - pathology | Acute Kidney Injury - enzymology | Sepsis - physiopathology | Acute Kidney Injury - physiopathology | Acute Kidney Injury - prevention & control | Animals | Electron Transport Complex II - metabolism | Sepsis - enzymology | Electron Transport Chain Complex Proteins - metabolism | Mice | Oxidative Stress - drug effects | Antioxidants | Superoxide | Genetic aspects | Health aspects
Journal Article
Kidney International, ISSN 0085-2538, 07/2012, Volume 82, Issue 1, pp. 45 - 52
To determine the role of epidermal growth factor receptor (EGFR) activation in renal functional and structural recovery from acute kidney injury (AKI), we... 
acute kidney injury | epidermal growth factor | proximal tubule | ischemia–reperfusion | ischemia-reperfusion | dialysis | parathyroid hormone | STEM-CELLS | ACTIVATION | EARLY PHASE | RAT-KIDNEY | renal osteodystrophy | REGENERATION | bone | MECHANISMS | FAILURE | ISCHEMIA-REPERFUSION INJURY | HYPERTROPHY | REPAIR | hemodialysis | UROLOGY & NEPHROLOGY | Erlotinib Hydrochloride | Receptor, Epidermal Growth Factor - genetics | Phosphorylation | Blood Urea Nitrogen | Receptor, Epidermal Growth Factor - deficiency | Acute Kidney Injury - genetics | Extracellular Signal-Regulated MAP Kinases - metabolism | Recovery of Function | Reperfusion Injury - blood | Time Factors | Gene Deletion | Kidney Tubules, Proximal - enzymology | Proto-Oncogene Proteins c-akt - metabolism | Phosphatidylinositol 3-Kinase - metabolism | Reperfusion Injury - genetics | Disease Models, Animal | Kidney Tubules, Proximal - physiopathology | Kidney Tubules, Proximal - pathology | Reperfusion Injury - pathology | Acute Kidney Injury - pathology | Reperfusion Injury - enzymology | Acute Kidney Injury - blood | Biomarkers - blood | Acute Kidney Injury - enzymology | Acute Kidney Injury - physiopathology | Mice, Knockout | Animals | Reperfusion Injury - physiopathology | Creatinine - blood | Mice | Mice, Inbred BALB C | Protein Kinase Inhibitors - pharmacology | Enzyme Activation | Quinazolines - pharmacology | Kidney Tubules, Proximal - drug effects | Original
Journal Article
American Journal of Physiology - Renal Physiology, ISSN 0363-6127, 05/2011, Volume 300, Issue 5, pp. 1180 - 1192
Wu QQ, Wang Y, Senitko M, Meyer C, Wigley WC, Ferguson DA, Grossman E, Chen J, Zhou XJ, Hartono J, Winterberg P, Chen B, Agarwal A, Lu CY. Bardoxolone methyl... 
Heme oxygenase 1 | Ischemia | Acute kidney injury | Cisplatin | CELLS | OXIDATIVE STRESS | PHYSIOLOGY | PROLIFERATOR-ACTIVATED RECEPTORS | REPERFUSION INJURY | 15-DEOXY-DELTA(12,14)-PROSTAGLANDIN J | ACUTE-RENAL-FAILURE | HEME OXYGENASE-1 GENE | ischemia | TRANSCRIPTION FACTOR NRF2 | UROLOGY & NEPHROLOGY | acute kidney injury | cisplatin | CHRONIC KIDNEY-DISEASE | DIRECT INHIBITION | heme oxygenase 1 | Up-Regulation | Heme Oxygenase-1 - metabolism | Kidney - blood supply | Kidney - pathology | Kidney - enzymology | Oleanolic Acid - analogs & derivatives | Ischemia - enzymology | Oleanolic Acid - pharmacology | Capillaries - drug effects | Male | Acute Kidney Injury - genetics | Ischemia - genetics | PPAR gamma - metabolism | RNA, Messenger - metabolism | Heme Oxygenase-1 - genetics | Time Factors | Ischemia - complications | NF-E2-Related Factor 2 - genetics | Membrane Proteins - metabolism | Acute Kidney Injury - etiology | Ischemia - pathology | Disease Models, Animal | PPAR gamma - genetics | Kidney - drug effects | Acute Kidney Injury - pathology | Membrane Proteins - genetics | Mice, Inbred C57BL | Acute Kidney Injury - enzymology | Capillaries - enzymology | Acute Kidney Injury - prevention & control | Animals | Analysis of Variance | Ischemia - drug therapy | NF-E2-Related Factor 2 - metabolism | Fluorescent Antibody Technique | Mice
Journal Article
American Journal of Physiology - Renal Physiology, ISSN 0363-6127, 06/2017, Volume 312, Issue 6, pp. F1166 - F1183
Acute kidney injury (AKI) causes severe morbidity, mortality, and chronic kidney disease (CKD). Mortality is particularly marked in the elderly and with... 
Innate immunity | Mitochondria | Chronic kidney disease | Acute kidney injury | Matrix metalloproteinase-2 | matrix metalloproteinase-2 | chronic kidney disease | PHYSIOLOGY | mitochondria | APOE MICE DEFICIENT | HEART-FAILURE | CELL-DEATH | ISCHEMIA-REPERFUSION INJURY | HYPERPOLARIZED C-13 DEHYDROASCORBATE | MURINE MODEL | MITOCHONDRIAL PERMEABILITY TRANSITION | innate immunity | INCREASED SUSCEPTIBILITY | IN-VIVO | UROLOGY & NEPHROLOGY | acute kidney injury | RENAL INJURY | Mitochondria - enzymology | Myocardial Infarction - genetics | Reactive Oxygen Species - metabolism | Age Factors | Kidney Tubular Necrosis, Acute - genetics | Oxidative Stress | Heart Failure - enzymology | Humans | Acute Kidney Injury - genetics | Coronary Artery Disease - enzymology | Mitochondria - ultrastructure | Necrosis | Kidney Tubular Necrosis, Acute - immunology | Myocardial Infarction - pathology | Coronary Artery Disease - pathology | Membrane Potential, Mitochondrial | Acute Kidney Injury - immunology | Kidney Tubules, Proximal - enzymology | Reperfusion Injury - genetics | Disease Models, Animal | Kidney Tubules, Proximal - ultrastructure | Myocardial Infarction - enzymology | Genetic Predisposition to Disease | Kidney Tubules, Proximal - immunology | Reperfusion Injury - pathology | Signal Transduction | Acute Kidney Injury - pathology | Isoenzymes | Kidney Tubular Necrosis, Acute - enzymology | Matrix Metalloproteinase 2 - metabolism | Reperfusion Injury - enzymology | Heart Failure - genetics | Mice, Transgenic | Heart Failure - pathology | Acute Kidney Injury - enzymology | Immunity, Innate | Mice, Knockout | Mitochondrial Degradation | Matrix Metalloproteinase 2 - genetics | Phenotype | Animals | Reperfusion Injury - immunology | Coronary Artery Disease - genetics | Kidney Tubular Necrosis, Acute - pathology | Development and progression | Kidney tubules | Health aspects | Metalloproteins | Acute renal failure
Journal Article
American Journal of Pathology, ISSN 0002-9440, 05/2009, Volume 174, Issue 5, pp. 1663 - 1674
Hypoxia-inducible transcription factors (HIFs) play important roles in the response of the kidney to systemic and regional hypoxia. Degradation of HIFs is... 
OXYGEN | CELLS | DOMAIN PROTEINS | ERYTHROPOIETIN | MESSENGER-RNA | HYPOXIA-INDUCIBLE-FACTOR | ACUTE-RENAL-FAILURE | INDUCTION | PATHOLOGY | UP-REGULATION | FACTOR-ALPHA | Fibroblasts - enzymology | Prognosis | Homeodomain Proteins - metabolism | Kidney - enzymology | Podocytes - enzymology | Male | Gene Expression Regulation, Enzymologic - physiology | RNA, Messenger - metabolism | Immunoenzyme Techniques | Oxygen - metabolism | Antineoplastic Agents - toxicity | Procollagen-Proline Dioxygenase - metabolism | DNA-Binding Proteins - metabolism | Immediate-Early Proteins - metabolism | Contrast Media - pharmacology | Cisplatin - toxicity | Hypoxia-Inducible Factor 1, alpha Subunit - metabolism | Kidney Tubules, Collecting - enzymology | Ischemia - pathology | Kidney Tubules, Collecting - drug effects | Kidney - drug effects | Kidney Medulla - enzymology | Kidney Tubules - drug effects | Kidney Medulla - drug effects | Mice, Inbred C57BL | RNA, Messenger - genetics | Ischemia - metabolism | Rats | Hypoxia-Inducible Factor-Proline Dioxygenases | Acute Kidney Injury - enzymology | DNA-Binding Proteins - genetics | Kidney - injuries | Reverse Transcriptase Polymerase Chain Reaction | Rats, Sprague-Dawley | Blotting, Western | Homeodomain Proteins - genetics | Animals | Immediate-Early Proteins - genetics | Podocytes - drug effects | Procollagen-Proline Dioxygenase - genetics | Kidney Tubules - enzymology | Fibroblasts - drug effects | Mice | Index Medicus | Abridged Index Medicus | Regular
Journal Article
Kidney International, ISSN 0085-2538, 02/2018, Volume 93, Issue 2, pp. 365 - 374
Ischemia/reperfusion is a common cause of acute kidney injury (AKI). However, mechanisms underlying the sudden loss in kidney function and tissue injury remain... 
neutrophil transfer | NETs | ischemia-reperfusion | PAD4 | AKI | PAD4 inhibitor | ACTIVATION | ACUTE-RENAL-FAILURE | RELEASE | CISPLATIN NEPHROTOXICITY | ISCHEMIA-REPERFUSION INJURY | LIVER-INJURY | DNA | INFLAMMATION | UROLOGY & NEPHROLOGY | EXTRACELLULAR TRAPS | CELL | Hydrolases - genetics | Kidney - pathology | Kidney - enzymology | Male | Neutrophil Infiltration | Inflammation Mediators - metabolism | Kidney - physiopathology | Disease Models, Animal | Neutrophils - pathology | Citrullination | Hydrolases - metabolism | Kidney - drug effects | Cytokines - metabolism | Neutrophils - enzymology | Reperfusion Injury - pathology | Acute Kidney Injury - pathology | Reperfusion Injury - enzymology | Mice, Inbred C57BL | Neutrophils - drug effects | Enzyme Inhibitors - pharmacology | Extracellular Traps - enzymology | Hydrolases - deficiency | Acute Kidney Injury - enzymology | Acute Kidney Injury - physiopathology | Acute Kidney Injury - prevention & control | Mice, Knockout | Animals | Reperfusion Injury - prevention & control | Neutrophils - transplantation | Histiocytes - metabolism | Reperfusion Injury - physiopathology | Hydrolases - antagonists & inhibitors | Deoxyribonuclease | Renal function | Kidneys | Cytokines | Leukocytes (neutrophilic) | Inflammation | Citrulline | Arginine deiminase | Reperfusion | Arginine | Ischemia | Protein-arginine deiminase | Histone H3
Journal Article
Journal Article