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1. Full Text LncRNA MALAT1 is dysregulated in diabetic nephropathy and involved in high glucose‐induced podocyte injury via its interplay with β‐catenin
by Hu, Mengsi and Wang, Rong and Li, Xiaobing and Fan, Minghua and Lin, Jiangong and Zhen, Junhui and Chen, Liqun and Lv, Zhimei
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
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2. Full Text Inhibition of high glucose-induced inflammation and fibrosis by a novel curcumin derivative prevents renal and heart injury in diabetic mice
by Chen, Hongjin and Yang, Xi and Lu, Kongqin and Lu, Chun and Zhao, Yunjie and Zheng, Suqing and Li, Jieli and Huang, Zhangjian and Huang, Yi and Zhang, Yali and Liang, Guang
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
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3. Full Text Cadmium, diabetes and chronic kidney disease
by Edwards, Joshua R and Prozialeck, Walter C
Toxicology and Applied Pharmacology, ISSN 0041-008X, 2009, Volume 238, Issue 3, pp. 289 - 293
Recent epidemiological studies suggest a positive association between exposure to the environmental pollutant cadmium (Cd) and the incidence and severity of... 
Cadmium | Fasting blood glucose | A1C | Diabetes | Insulin | POPULATION | RATS | LEVEL | RENAL DYSFUNCTION | METALS | GLUCOSE-METABOLISM | URINARY CADMIUM | PHARMACOLOGY & PHARMACY | TOXICOLOGY | ASSOCIATION | EXPOSURE | NEPHROTOXICITY | Cadmium - toxicity | Risk Assessment | Diabetic Nephropathies - etiology | Diabetic Nephropathies - metabolism | Humans | Risk Factors | Diabetic Nephropathies - chemically induced | Diabetes Mellitus - metabolism | Pancreas - drug effects | Pancreas - pathology | Pancreas - metabolism | Insulin - blood | Blood Glucose - drug effects | Animals | Diabetes Mellitus - epidemiology | Diabetes Mellitus - chemically induced | Models, Animal | Diabetic Nephropathies - epidemiology | Environmental Pollutants - toxicity | Chronic Disease | Hyperglycemia | Blood sugar | Analysis | Diabetic nephropathies | Index Medicus | ANIMALS | HUMAN POPULATIONS | POLLUTANTS | PANCREAS | UROGENITAL SYSTEM DISEASES | 60 APPLIED LIFE SCIENCES | INSULIN | KIDNEYS | HYPERGLYCEMIA | CADMIUM | GLUCOSE | DIABETES MELLITUS | BLOOD | cadmium | fasting blood glucose | insulin | diabetes
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4. Full Text MicroRNA-27a promotes podocyte injury via PPARγ-mediated β-catenin activation in diabetic nephropathy
by Zhou, Zhanmei and Wan, Jiao and Hou, Xiaoyan and Geng, Jian and Li, Xiao and Bai, Xiaoyan
Cell Death and Disease, ISSN 2041-4889, 2017, Volume 8, Issue 3, pp. e2658 - e2658
Podocyte injury has a pivotal role in the pathogenesis of diabetic nephropathy (DN). MicroRNA-27a (miR-27a), peroxisome proliferator-activated receptor gamma... 
KIDNEY-DISEASE | TO-MESENCHYMAL TRANSITION | PATHWAY | PHOSPHORYLATION | DOWNSTREAM | RETINOPATHY | MICE | AGONIST ROSIGLITAZONE | DYSFUNCTION | ADIPOGENESIS | CELL BIOLOGY | Diabetic Nephropathies - pathology | Podocytes - metabolism | Diabetic Nephropathies - metabolism | Humans | Transcriptional Activation | Diabetes Mellitus, Experimental - genetics | Diabetic Nephropathies - chemically induced | Gene Expression Regulation | Rats | Diabetic Nephropathies - genetics | Male | Podocytes - pathology | Cell Movement - genetics | beta Catenin - genetics | Actins - genetics | Animals | Wnt Signaling Pathway - genetics | Glucose - toxicity | Diabetes Mellitus, Experimental - chemically induced | MicroRNAs - genetics | Diabetes Mellitus, Experimental - physiopathology | PPAR gamma - genetics | Original
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5. Full Text Defective podocyte insulin signalling through p85-XBP1 promotes ATF6-dependent maladaptive ER-stress response in diabetic nephropathy
by Madhusudhan, Thati and Wang, Hongjie and Dong, Wei and Ghosh, Sanchita and Bock, Fabian and Thangapandi, Veera Raghavan and Ranjan, Satish and Wolter, Juliane and Kohli, Shrey and Shahzad, Khurrum and Heidel, Florian and Krueger, Martin and Schwenger, Vedat and Moeller, Marcus J and Kalinski, Thomas and Reiser, Jochen and Chavakis, Triantafyllos and Isermann, Berend
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
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6. Full Text High glucose-induced O-GlcNAcylated Carbohydrate response element-binding protein (ChREBP) mediates mesangial cell lipogenesis and fibrosis the possible role in the development of diabetic nephropathy
by Park, Min-Jung and Kim, Dong-Il and Lim, Seul-Ki and Choi, Joo-Hee and Han, Ho-Jae and Yoon, Kyung-Chul and Park, Soo-Hyun
Journal of Biological Chemistry, ISSN 0021-9258, 1768, Volume 289, Issue 19, pp. 13519 - 13530
Carbohydrate response element-binding protein (ChREBP) is a transcription factor responsible for carbohydrate metabolism in the liver. However, the role of... 
Gene Expression Regulation, Enzymologic - drug effects | Triglycerides - biosynthesis | Humans | Diabetes Mellitus, Experimental - genetics | Fibrosis - metabolism | Cholesterol - genetics | HEK293 Cells | Acetylglucosamine - analogs & derivatives | Diabetes Mellitus, Experimental - metabolism | Diabetic Nephropathies - pathology | Fibrosis - genetics | Fibrosis - chemically induced | Sweetening Agents - pharmacology | Diabetic Nephropathies - metabolism | Diabetic Nephropathies - chemically induced | Rats | Acetylglucosamine - pharmacology | Diabetic Nephropathies - genetics | Glucose - pharmacology | Mesangial Cells - metabolism | beta-N-Acetylhexosaminidases - biosynthesis | Phenylcarbamates - pharmacology | Animals | Gene Expression Regulation, Enzymologic - genetics | Lipogenesis - drug effects | Basic Helix-Loop-Helix Leucine Zipper Transcription Factors - genetics | Mesangial Cells - pathology | Diabetes Mellitus, Experimental - pathology | Oximes - pharmacology | Basic Helix-Loop-Helix Leucine Zipper Transcription Factors - metabolism | Fibrosis - pathology | Triglycerides - genetics | Cholesterol - biosynthesis | Molecular Bases of Disease | O-GlcNAcylation | Kidney Metabolism | Diabetes | Lipogenesis | Fibrosis
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7. Full Text NADPH oxidase NOX1 is involved in activation of protein kinase C and premature senescence in early stage diabetic kidney
by Zhu, Kai and Kakehi, Tomoko and Matsumoto, Misaki and Iwata, Kazumi and Ibi, Masakazu and Ohshima, Yoichi and Zhang, Jia and Liu, Junjie and Wen, Xiaopeng and Taye, Ashraf and Fan, Chunyuan and Katsuyama, Masato and Sharma, Kumar and Yabe-Nishimura, Chihiro
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
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8. Full Text Lycium barbarum polysaccharides ameliorates renal injury and inflammatory reaction in alloxan-induced diabetic nephropathy rabbits
by Zhao, Qihan and Li, Jingjing and Yan, Jun and Liu, Shuai and Guo, Yulin and Chen, Dajie and Luo, Qiong
Life Sciences, ISSN 0024-3205, 07/2016, Volume 157, pp. 82 - 90
This study was aimed to investigate the effect of polysaccharides (LBP) on renal function and inflammatory reaction in rabbits with diabetic nephropathy.... 
Lycium barbarum polysaccharides | Diabetic nephropathy | Renal function | Inflammatory reaction | MEDICINE, RESEARCH & EXPERIMENTAL | CELLS | REPRODUCTIVE-SYSTEM | INTERSTITIAL INFLAMMATION | RATS | ANGIOTENSIN-II | IRRADIATION | INHIBITION | INSULIN-RESISTANCE | PHARMACOLOGY & PHARMACY | CHEMOATTRACTANT PROTEIN-1 | MICE | Rabbits | Kidney - drug effects | Diabetic Nephropathies - chemically induced | Body Weight - drug effects | Male | Polysaccharides - pharmacology | Alloxan | Intercellular Adhesion Molecule-1 - metabolism | Kidney - metabolism | Organ Size - drug effects | Animals | Chemokine CCL2 - metabolism | Inflammation - prevention & control | Blood Glucose - metabolism | Diabetic Nephropathies - prevention & control | Lycium - chemistry | Pyrimidines | Polysaccharides | Diabetic nephropathies | Prevention | Urea | RNA | Analysis | Telmisartan
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9. Full Text Empagliflozin, an Inhibitor of Sodium-Glucose Cotransporter 2 Exerts Anti-Inflammatory and Antifibrotic Effects on Experimental Diabetic Nephropathy Partly by Suppressing AGEs-Receptor Axis
by Ojima, A and Matsui, T and Nishino, Y and Nakamura, N and Yamagishi, S
Hormone and Metabolic Research, ISSN 0018-5043, 08/2015, Volume 47, Issue 9, pp. 686 - 692
Abstract Abstract Advanced glycation end products (AGEs) and receptor RAGE play a role in diabetic nephropathy. We have previously shown that increased glucose... 
Endocrine Research | AGEs | RAGE | SGLT2 | diabetic nephropathy | oxidative stress | GLOMERULOSCLEROSIS | GLYCEMIC CONTROL | GLOMERULAR HYPERFILTRATION | TUBULAR CELL INJURY | ENDOCRINOLOGY & METABOLISM | KIDNEY | BIOCHEMICAL BASIS | GLYCATION END-PRODUCTS | Diabetes Mellitus, Experimental - drug therapy | Glucosides - pharmacology | Gene Expression - drug effects | Fibromyalgia - prevention & control | Diabetic Nephropathies - chemically induced | Diabetic Nephropathies - drug therapy | Rats | Male | Glycation End Products, Advanced - drug effects | Rats, Sprague-Dawley | Sodium-Glucose Transporter 2 - antagonists & inhibitors | Hypoglycemic Agents - pharmacology | Animals | Benzhydryl Compounds - pharmacology | Diabetes Mellitus, Experimental - chemically induced | Inflammation - prevention & control | Receptor for Advanced Glycation End Products - drug effects | Oxidative Stress - drug effects
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10. Full Text Metallothionein plays a prominent role in the prevention of diabetic nephropathy by sulforaphane via up-regulation of Nrf2
by Wu, Hao and Kong, Lili and Cheng, Yanli and Zhang, Zhiguo and Wang, Yangwei and Luo, Manyu and Tan, Yi and Chen, Xiangmei and Miao, Lining and Cai, Lu
Free Radical Biology and Medicine, ISSN 0891-5849, 12/2015, Volume 89, pp. 431 - 442
Sulforaphane (SFN) prevents diabetic nephropathy (DN) in type 1 diabetes via up-regulation of nuclear factor (erythroid-derived 2)-like 2 (Nrf2). However, it... 
Oxidative stress | Inflammation | Diabetes | Kidney | Fibrosis | Diabetic Nephropathies - pathology | Oxidative Stress | Diabetic Nephropathies - metabolism | Mice, Inbred C57BL | RNA, Messenger - genetics | Diabetic Nephropathies - chemically induced | Male | Reverse Transcriptase Polymerase Chain Reaction | Blotting, Western | Immunoenzyme Techniques | Mice, Knockout | Isothiocyanates - toxicity | Animals | Diabetes Mellitus, Type 2 - physiopathology | Anticarcinogenic Agents - toxicity | Metallothionein - pharmacology | NF-E2-Related Factor 2 - metabolism | NF-E2-Related Factor 2 - genetics | Diabetes Mellitus, Experimental - complications | Mice | Diabetic Nephropathies - prevention & control | Real-Time Polymerase Chain Reaction | Diabetes Mellitus, Type 2 - complications | Diabetes Mellitus, Experimental - physiopathology | Prevention | Antioxidants | Kidney diseases | Metallothionein
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11. Full Text Momordica charantia polysaccharides mitigate the progression of STZ induced diabetic nephropathy in rats
by Raish, Mohammad and Ahmad, Ajaz and Jan, Basit L and Alkharfy, Khalid M and Ansari, Mushtaq Ahmad and Mohsin, Kazi and Jenoobi, Fahad al and Al-Mohizea, Abdullah
International Journal of Biological Macromolecules, ISSN 0141-8130, 10/2016, Volume 91, pp. 394 - 399
Diabetic nephropathy (DN) has become a primary cause of end-stage kidney disease. Several complex dynamics converge together to accelerate the advancement of... 
Momordica charantia | Polysaccharides | Diabetic nepropathy | OXIDATIVE STRESS | POLYMER SCIENCE | EFFICACY | BIOCHEMISTRY & MOLECULAR BIOLOGY | INJURY | MELLITUS | NRF2 | SIGNALING PATHWAY | MICE | CHEMISTRY, APPLIED | NF-KAPPA-B | EXPRESSION | ALDOSE REDUCTASE | Diabetes Mellitus, Experimental - drug therapy | Heme Oxygenase-1 - metabolism | Diabetic Nephropathies - metabolism | Momordica charantia - chemistry | Diabetic Nephropathies - chemically induced | Diabetic Nephropathies - drug therapy | Rats | Male | Polysaccharides - pharmacology | Kidney - metabolism | Animals | Signal Transduction - drug effects | NF-E2-Related Factor 2 - metabolism | Polysaccharides - chemistry | Oxidative Stress - drug effects | Diabetes Mellitus, Experimental - metabolism | Antioxidants | Drugstores | Enzymes | Pharmacy | Diabetic nephropathies | Urea | Hyperglycemia | Chronic kidney failure | Heme | Index Medicus
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12. Full Text CXCL8 antagonist improves diabetic nephropathy in male mice with diabetes and attenuates high glucose-induced mesangial injury
by Cui, Siyuan and Zhu, Yujie and Du, Jianling and Khan, Muhammad Noman and Wang, Bing and Wei, Jing and Cheng, Jya-Wei and Gordon, John R and Mu, Yutian and Li, Fang
Endocrinology, ISSN 0013-7227, 06/2017, Volume 158, Issue 6, pp. 1671 - 1684
Inflammation is recognized as a crucial contribution to diabetic nephropathy (DN). CXCL8 binds to its CXC chemokine receptors (CXCR1 and CXCR2) for recruiting... 
KIDNEY-DISEASE | FIBROSIS | LYMPHOCYTE RATIO | ACTIVATION | GROWTH-FACTOR VEGF | INFLAMMATION | ENDOCRINOLOGY & METABOLISM | CELL PROLIFERATION | RECEPTOR | RENAL-DISEASE | COMPLICATIONS | Diabetes Mellitus, Experimental - drug therapy | Diabetic Nephropathies - pathology | Streptozocin | Mice, Inbred C57BL | Diabetic Nephropathies - chemically induced | Male | Peptide Fragments - pharmacology | Interleukin-8 - antagonists & inhibitors | Hypoglycemic Agents - pharmacology | Mesangial Cells - drug effects | Dose-Response Relationship, Drug | Animals | Mesangial Cells - pathology | Glucose - toxicity | Interleukin-8 - pharmacology | Diabetes Mellitus, Experimental - complications | Mice | Diabetic Nephropathies - prevention & control | Glucose | Inflammatory diseases | High fat diet | Antagonism | Receptors | Rodents | Janus kinase 2 | Mesangial cells | Extracellular matrix | Attenuation | Inhibition | CXC chemokine receptors | Urine | Creatinine | Kidneys | CXCR2 protein | Diabetes mellitus | Stat3 protein | Extracellular signal-regulated kinase | Inflammation | Chemokine receptors | White blood cells | Urea | Signaling | Cell injury | Nephropathy | Fibrosis | Infiltration | Diabetes | Kidney transplantation
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13. Full Text Inhibition of MAPK‐mediated ACE expression by compound C66 prevents STZ‐induced diabetic nephropathy
by Pan, Yong and Huang, Yi and Wang, Zhe and Fang, Qilu and Sun, Yusheng and Tong, Chao and Peng, Kesong and Wang, Yangwei and Miao, Lining and Cai, Lu and Zhao, Yunjie and Liang, Guang
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 |