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Journal of Cellular and Molecular Medicine, ISSN 1582-1838, 11/2017, Volume 21, Issue 11, pp. 2732 - 2747
Metastasis associated lung adenocarcinoma transcript 1( MALAT 1) is a long non‐coding RNA , broadly expressed in mammalian tissues including kidney and... 
MALAT | β‐catenin | SRSF | high glucose | diabetic nephropathy | podocyte | β-catenin | MALAT1 | SRSF1 | beta-catenin | MEDICINE, RESEARCH & EXPERIMENTAL | APOPTOSIS | RETAINED NONCODING RNA | PROLIFERATION | MESENCHYMAL TRANSITION | CELL BIOLOGY | GLOMERULAR SLIT DIAPHRAGM | ROLES | DYSFUNCTION | WNT | SPLICING FACTOR | RNA, Small Interfering - genetics | Diabetes Mellitus, Experimental - genetics | Male | Serine-Arginine Splicing Factors - metabolism | Serine-Arginine Splicing Factors - genetics | Glucose - toxicity | Diabetes Mellitus, Experimental - chemically induced | Diabetes Mellitus, Experimental - metabolism | Wnt Signaling Pathway | Promoter Regions, Genetic | Diabetic Nephropathies - pathology | Podocytes - metabolism | Diabetic Nephropathies - metabolism | Mice, Inbred C57BL | Diabetic Nephropathies - chemically induced | Gene Expression Regulation | Diabetic Nephropathies - genetics | RNA, Long Noncoding - genetics | Podocytes - pathology | beta Catenin - metabolism | beta Catenin - genetics | Protein Transport | Serine-Arginine Splicing Factors - antagonists & inhibitors | Feedback, Physiological | Animals | Podocytes - drug effects | beta Catenin - antagonists & inhibitors | Diabetes Mellitus, Experimental - pathology | Protein Binding | Mice | Streptozocin - toxicity | RNA, Long Noncoding - antagonists & inhibitors | RNA, Long Noncoding - metabolism | Cell Line, Transformed | RNA, Small Interfering - metabolism | Original
Journal Article
Toxicology Letters, ISSN 0378-4274, 08/2017, Volume 278, pp. 48 - 58
Hyperglycemia-induced inflammation and fibrosis have important roles in the pathogenesis of diabetic nephropathy and cardiomyopathy. With inflammatory... 
Diabetic cardiomyopathy | Diabetic nephropathy | Curcumin | Anti-inflammation | Fibrosis | ANALOGS | CARDIOMYOPATHY | ACUTE LUNG INJURY | NEPHROPATHY | ANTIINFLAMMATORY AGENTS | ATTENUATION | TUBULAR EPITHELIAL-CELLS | COMPLICATIONS | TOXICOLOGY | DYSFUNCTION | KIDNEY | Curcumin - analogs & derivatives | Diabetes Mellitus, Experimental - drug therapy | Diabetic Cardiomyopathies - metabolism | Kidney - pathology | Streptozocin | Male | Kidney - metabolism | Time Factors | Inflammation Mediators - metabolism | Diabetic Cardiomyopathies - prevention & control | Diabetes Mellitus, Experimental - chemically induced | p38 Mitogen-Activated Protein Kinases - metabolism | Diabetes Mellitus, Experimental - metabolism | Proto-Oncogene Proteins c-akt - metabolism | Diabetic Nephropathies - prevention & control | Cell Line | Diabetic Nephropathies - pathology | Kidney - drug effects | Cytokines - metabolism | Anti-Inflammatory Agents - pharmacology | Diabetic Nephropathies - metabolism | Mice, Inbred C57BL | Curcumin - pharmacology | Diabetic Nephropathies - chemically induced | Myocytes, Cardiac - pathology | Animals | Myocytes, Cardiac - drug effects | Signal Transduction - drug effects | Diabetes Mellitus, Experimental - pathology | Myocytes, Cardiac - metabolism | Diabetic Cardiomyopathies - pathology | Blood Glucose - metabolism | Diabetic Cardiomyopathies - chemically induced | Prevention | Hyperglycemia | Analysis | Diabetic nephropathies | Inflammation | Glucose | Health aspects | Dextrose | Index Medicus
Journal Article
Journal Article
Nature Communications, ISSN 2041-1723, 03/2015, Volume 6, Issue 1, p. 6496
Endoplasmic reticulum (ER) stress is associated with diabetic nephropathy (DN), but its pathophysiological relevance and the mechanisms that compromise... 
KIDNEY-DISEASE | GLUCOSE-HOMEOSTASIS | XBP1 | UNFOLDED PROTEIN RESPONSE | GLOMERULAR PODOCYTE | ENDOPLASMIC-RETICULUM-STRESS | BOX-BINDING PROTEIN-1 | REGULATORY SUBUNITS | MULTIDISCIPLINARY SCIENCES | MICE | METABOLIC-DISORDERS | Transcription Factor CHOP - genetics | Streptozocin | Humans | Transcription Factors - deficiency | Diabetes Mellitus, Experimental - genetics | Receptor, Insulin - deficiency | Endoplasmic Reticulum - metabolism | Male | Endoplasmic Reticulum Stress - genetics | Activating Transcription Factor 6 - genetics | DNA-Binding Proteins - deficiency | X-Box Binding Protein 1 | Endoplasmic Reticulum - pathology | Class Ia Phosphatidylinositol 3-Kinase - deficiency | Receptor, Insulin - genetics | Diabetes Mellitus, Experimental - chemically induced | Class Ia Phosphatidylinositol 3-Kinase - genetics | Diabetes Mellitus, Experimental - metabolism | Databases, Factual | Diabetic Nephropathies - pathology | Podocytes - metabolism | Endoplasmic Reticulum - genetics | Signal Transduction | Diabetic Nephropathies - metabolism | Mice, Inbred C57BL | Diabetic Nephropathies - chemically induced | Gene Expression Regulation | Diabetic Nephropathies - genetics | Podocytes - pathology | Transcription Factors - genetics | DNA-Binding Proteins - genetics | Activating Transcription Factor 6 - deficiency | Regulatory Factor X Transcription Factors | Mice, Knockout | Insulin - metabolism | Animals | Diabetes Mellitus, Experimental - pathology | Mice | Transcription Factor CHOP - metabolism
Journal Article
Journal of Biological Chemistry, ISSN 0021-9258, 1768, Volume 289, Issue 19, pp. 13519 - 13530
Journal Article
Free Radical Biology and Medicine, ISSN 0891-5849, 06/2015, Volume 83, pp. 21 - 30
Increased oxidative stress and activation of protein kinase C (PKC) under hyperglycemia have been implicated in the development of diabetic nephropathy.... 
Diabetic nephropathy | Protein kinase C | Senescence | Free radicals | NADPH oxidase | NOX1 | PHOSPHORYLATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | NEPHROPATHY | P27(KIP1) | INHIBITION | NOX1/NADPH OXIDASE | ENDOCRINOLOGY & METABOLISM | CELL-CYCLE | COMPLICATIONS | MICE | HYPERTENSION | EXPRESSION | Protein Kinase C - genetics | Reactive Oxygen Species - metabolism | Oxidative Stress | Male | Immunoenzyme Techniques | NADH, NADPH Oxidoreductases - physiology | Hyperglycemia - chemically induced | Glomerular Mesangium - metabolism | Protein Kinase C - metabolism | Hyperglycemia - pathology | beta-Galactosidase - metabolism | Diabetes Mellitus, Experimental - chemically induced | p38 Mitogen-Activated Protein Kinases - metabolism | Diabetes Mellitus, Experimental - metabolism | Real-Time Polymerase Chain Reaction | Diabetic Nephropathies - pathology | Oxidation-Reduction | Signal Transduction | Diabetic Nephropathies - metabolism | Mice, Inbred C57BL | RNA, Messenger - genetics | Cells, Cultured | Diabetic Nephropathies - chemically induced | Cellular Senescence - physiology | p38 Mitogen-Activated Protein Kinases - genetics | Reverse Transcriptase Polymerase Chain Reaction | Blotting, Western | NADPH Oxidase 1 | Mice, Knockout | Hyperglycemia - metabolism | Glomerular Mesangium - pathology | Animals | Diabetes Mellitus, Experimental - pathology | Mice | Oxidases | Phosphates | Niacinamide | Purines | Hyperglycemia | RNA | Diabetic nephropathies | Development and progression | Protein kinases
Journal Article
Journal Article
Journal Article
Journal Article
Endocrinology, ISSN 0013-7227, 06/2017, Volume 158, Issue 6, pp. 1671 - 1684
Journal Article
Journal of Cellular and Molecular Medicine, ISSN 1582-1838, 02/2014, Volume 18, Issue 2, pp. 231 - 241
A range of in vitro , experimental and clinical intervention studies have implicated an important role for hyperglycaemia‐induced activation of the... 
mitogen‐activated protein kinases | (2E,6E)‐2,6‐bis(2‐(trifluoromethyl)benzylidene)cyclohexanone | angiotensin converting enzyme | renin‐angiotensin system | diabetic nephropathy | Diabetic nephropathy | (2E,6E)-2,6-bis(2-(trifluoromethyl)benzylidene)cyclohexanone | Renin-angiotensin system | Angiotensin converting enzyme | Mitogen-activated protein kinases | SYSTEM | MEDICINE, RESEARCH & EXPERIMENTAL | ACTIVATED PROTEIN-KINASE | RECEPTOR BLOCKADE | 6E)-2 | TRANSCRIPTION | INJURY | MESENCHYMAL TRANSITION | ANGIOTENSIN-CONVERTING ENZYME | 6-bis(2-(trifluoromethyl)benzylidene)cyclohexanone | CELL BIOLOGY | 2E | mitogen-activated protein kinases | ENDOTHELIAL-CELLS | HIGH GLUCOSE | GENE-EXPRESSION | renin-angiotensin system | Diabetes Mellitus, Experimental - drug therapy | Angiotensin II - genetics | Kidney - pathology | Streptozocin | Male | Hyperglycemia - drug therapy | Peptidyl-Dipeptidase A - genetics | Kidney - metabolism | Hyperglycemia - chemically induced | Hyperglycemia - pathology | Peptidyl-Dipeptidase A - metabolism | Diabetes Mellitus, Experimental - chemically induced | Diabetes Mellitus, Experimental - metabolism | Diabetic Nephropathies - prevention & control | Diabetic Nephropathies - pathology | Kidney - drug effects | Angiotensin II - metabolism | Signal Transduction | Diabetic Nephropathies - metabolism | Mice, Inbred C57BL | Diabetic Nephropathies - chemically induced | Gene Expression Regulation | Renin-Angiotensin System - genetics | Cyclohexanones - pharmacology | Hyperglycemia - metabolism | Animals | Benzylidene Compounds - pharmacology | Mitogen-Activated Protein Kinases - antagonists & inhibitors | Diabetes Mellitus, Experimental - pathology | Mitogen-Activated Protein Kinases - genetics | Renin-Angiotensin System - drug effects | Mice | Protein Kinase Inhibitors - pharmacology | Mitogen-Activated Protein Kinases - metabolism | Prevention | Glucose metabolism | Hyperglycemia | Blood sugar | Analysis | Diabetic nephropathies | Angiotensin | Genetic research |