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Journal Article
American Journal of Physiology - Endocrinology And Metabolism, ISSN 0193-1849, 02/2010, Volume 298, Issue 2, pp. 210 - 221
Cells exposed to high glucose may undergo hypertrophy, proliferation, and apoptosis, but the role of hexosamine flux in mediating these effects has not been... 
Hexosamine flux | Cell turnover | High glucose | MAMMALIAN TARGET | APOPTOSIS | PHYSIOLOGY | PROTEIN-KINASE | CYCLE ARREST | hexosamine flux | DIABETIC-NEPHROPATHY | high glucose | BETA-N-ACETYLGLUCOSAMINE | SIGNALING PATHWAY | ENDOCRINOLOGY & METABOLISM | REPLICATION FORK | O-GLCNAC | cell turnover | GLUTAMINE-FRUCTOSE-6-PHOSPHATE AMIDOTRANSFERASE | Adaptation, Physiological | Apoptosis - drug effects | Intracellular Signaling Peptides and Proteins - metabolism | Glucosamine - metabolism | Glucose - administration & dosage | Mesangial Cells - drug effects | Dose-Response Relationship, Drug | Hyperglycemia - physiopathology | Protein-Serine-Threonine Kinases - metabolism | Biosynthetic Pathways - physiology | Cells, Cultured | Rats | Mesangial Cells - metabolism | Rats, Sprague-Dawley | Glucosamine - administration & dosage | Hyperglycemia - metabolism | Carbohydrate Metabolism - physiology | Animals | Biosynthetic Pathways - drug effects | Cell Cycle - physiology | Glucose - metabolism | Glutamine-Fructose-6-Phosphate Transaminase (Isomerizing) - metabolism | Cell Proliferation - drug effects | TOR Serine-Threonine Kinases | Apoptosis - physiology | Cell Cycle - drug effects | Proliferating Cell Nuclear Antigen - metabolism | Glucosamine | Hyperglycemia | Care and treatment | Physiological aspects | Research | Risk factors | Apoptosis
Journal Article
Diabetes, ISSN 0012-1797, 04/2002, Volume 51, Issue 4, pp. 1146 - 1156
Flux Through the Hexosamine Pathway Is a Determinant of Nuclear Factor κB– Dependent Promoter Activation Leighton R. James 1 , Damu Tang 2 , Alistair Ingram 2... 
CELL-ADHESION MOLECULE-1 | TRANSCRIPTION FACTORS | TUMOR-NECROSIS-FACTOR | GLOMERULAR MESANGIAL CELLS | O-GLYCOSYLATION | ENDOTHELIAL-CELLS | ENDOCRINOLOGY & METABOLISM | GENE-EXPRESSION | SMOOTH-MUSCLE CELLS | GLUTAMINE-FRUCTOSE-6-PHOSPHATE AMIDOTRANSFERASE | FACTOR-ALPHA
Journal Article
by Suh, SH and Choi, HS and Kim, CS and Kim, IJ and Ma, SK and Scholey, JW and Kim, SW and Bae, EH
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, ISSN 1422-0067, 08/2019, Volume 20, Issue 15, p. 3843
Despite the wide use of angiotensin II receptor blockers in the treatment of Alport syndrome (AS), the mechanism as to how angiotensin II receptor blockers... 
olmesartan | transforming growth factor beta | BIOCHEMISTRY & MOLECULAR BIOLOGY | IV COLLAGEN | MEDOXOMIL | CHEMISTRY, MULTIDISCIPLINARY | ANGIOTENSIN-CONVERTING ENZYME-2 | RECEPTOR BLOCKER | ACE2 | INHIBITION | THERAPY | Alport syndrome | DISEASE | angiotensin-converting enzyme 2 | MICE | renin-angiotensin system | BASEMENT-MEMBRANE | ras Proteins - genetics | Antihypertensive Agents - pharmacology | Nephritis, Hereditary - pathology | Tetrazoles - pharmacology | Apoptosis - drug effects | ras Proteins - metabolism | Peptidyl-Dipeptidase A - genetics | Peptidyl-Dipeptidase A - metabolism | Kidney Tubules - pathology | Kidney Tubules - metabolism | Disease Models, Animal | Kidney Tubules - drug effects | Nephritis, Hereditary - genetics | Treatment Outcome | Imidazoles - pharmacology | Mice, Knockout | Gene Expression Regulation - drug effects | Animals | Nephritis, Hereditary - metabolism | Transforming Growth Factor beta - genetics | Biopsy | Fibrosis | Biomarkers | Mice | Nephritis, Hereditary - drug therapy | Transforming Growth Factor beta - metabolism | Urine | Myocardial infarction | Creatinine | Cerebral infarction | Enzymes | Phosphorylation | Animal models | Kidneys | Cardiomyopathy | Body weight | Neutrophils | Albumin | Inflammation | Kinases | Albumins | Dilated cardiomyopathy | Collagen | Myosin | Blood pressure | Age | Apoptosis | transforming growth factor β
Journal Article
Journal Article
PLoS ONE, ISSN 1932-6203, 08/2013, Volume 8, Issue 8, p. e71433
Ischemia-reperfusion (I/R) is a model of acute kidney injury (AKI) that is characterized by vasoconstriction, oxidative stress, apoptosis and inflammation.... 
SYSTEM | ISCHEMIA/REPERFUSION INJURY | ACTIVATION | INHIBITION | MULTIDISCIPLINARY SCIENCES | MOUSE MODEL | KIDNEY | RECEPTORS | ANGIOTENSIN-CONVERTING ENZYME | EXPRESSION | FAILURE | Inflammation - pathology | Kidney - pathology | Oxidative Stress | Chemokine CCL2 - immunology | Kidney - enzymology | Tumor Necrosis Factor-alpha - genetics | Kidney - immunology | Male | Interleukin-1beta - genetics | Neutrophil Infiltration | Peptidyl-Dipeptidase A - genetics | Tumor Necrosis Factor-alpha - immunology | Chemokine CXCL2 - genetics | T-Lymphocytes - pathology | Macrophages - immunology | Neutrophils - pathology | Gene Expression | Angiotensin II - metabolism | Interleukin-6 - genetics | Macrophages - pathology | Reperfusion Injury - pathology | Renin-Angiotensin System - immunology | Reperfusion Injury - enzymology | Neutrophils - immunology | Interleukin-1beta - immunology | Chemokine CCL2 - genetics | Inflammation - immunology | Mice, Knockout | Chemokine CXCL2 - immunology | Animals | Reperfusion Injury - immunology | Interleukin-6 - immunology | T-Lymphocytes - immunology | Mice | Peptidyl-Dipeptidase A - immunology | Inflammation - enzymology | Chronic kidney failure | Ischemia | RNA | Analysis | Angiotensin converting enzyme | Angiotensin | Inflammation | T cells | Apoptosis | Oxidative stress | Animal models | Nephrology | Transplants & implants | Syngeneic grafts | Interleukin | Science | Lymphocytes T | mRNA | Kinases | Macrophages | Angiotensin-converting enzyme 2--ACE2 | Metastases | Interleukin 6 | Reperfusion | Renin | Health care networks | Tumor necrosis factor-TNF | Angiotensin II | Injuries | Enzymes | Departments | Cytokines | Vasoconstriction | Histology | Gene expression | Macrophage inflammatory protein 2 | Medicine | Tumor necrosis factor | Monocyte chemoattractant protein | Infiltration | Kidney diseases | Diabetes | Macrophage inflammatory protein | Chemokines | Monocyte chemoattractant protein 1 | Tumors | Angiotensin-converting enzyme 2 | ACE2
Journal Article
American Journal of Physiology - Renal Physiology, ISSN 0363-6127, 2013, Volume 304, Issue 11, pp. 1366 - 1374
Obesity is a risk factor for chronic kidney disease (CKD) progression. Circulating levels of adiponectin, an adipokine, decrease with obesity and play a... 
Obesity | AMPK | Chronic kidney disease | Adipokine | cAMP | PROTEIN-KINASE-A | LEPTIN | chronic kidney disease | ACTIVATION | PHYSIOLOGY | adipokine | INDUCED APOPTOSIS | ALBUMINURIA | RECEPTOR | ENDOTHELIAL-CELLS | UROLOGY & NEPHROLOGY | CAMP/PROTEIN KINASE | KIDNEY | obesity | AMP-Activated Protein Kinases - metabolism | Humans | Kidney Tubules, Proximal - chemistry | AMP-Activated Protein Kinases - drug effects | Drug Interactions | Guanine Nucleotide Exchange Factors - metabolism | Cyclic AMP - metabolism | NF-kappa B - analysis | Pyrazoles - pharmacology | Adiponectin - pharmacology | Angiotensin II - pharmacology | Gene Expression | NF-kappa B - antagonists & inhibitors | AMP-Activated Protein Kinases - antagonists & inhibitors | NADPH Oxidases - antagonists & inhibitors | Cells, Cultured | Enzyme Inhibitors - pharmacology | Renin-Angiotensin System - physiology | Pyrimidines - pharmacology | Enzyme Activation - drug effects | Fibronectins - antagonists & inhibitors | Renal Insufficiency, Chronic - prevention & control | Signal Transduction - drug effects | Kidney Tubules, Proximal - metabolism | NF-kappa B - physiology | Renin-Angiotensin System - drug effects | Oxidative Stress - drug effects | Angiotensin II - physiology | Receptors, Adiponectin - genetics | Kidney Tubules, Proximal - drug effects | Fibronectins | Oxidative stress | Care and treatment | Chronic kidney failure | Physiological aspects | Development and progression | Genetic aspects | Research
Journal Article