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1. Full Text Regulation of ROS Signal Transduction by NADPH Oxidase 4 Localization
by Kai Chen and Michael T. Kirber and Hui Xiao and Yu Yang and John F. Keaney
The Journal of Cell Biology, ISSN 0021-9525, 6/2008, Volume 181, Issue 7, pp. 1129 - 1139
Reactive oxygen species (ROS) function as intracellular signaling molecules in a diverse range of biological processes. However, it is unclear how freely... 
COS cells | Oxidases | Reactive oxygen species | Phosphorylation | Receptors | Smooth muscle myocytes | Antibodies | Oxidation | Physiological regulation | Endothelial cells | GROWTH-FACTOR RECEPTOR | NAD(P)H OXIDASE | OXIDATIVE STRESS | TYROSINE-PHOSPHATASE 1B | NITRIC-OXIDE SYNTHASE | ENDOTHELIAL-CELLS | SMOOTH-MUSCLE-CELLS | ENDOPLASMIC-RETICULUM | HYDROGEN-PEROXIDE | KINASE ACTIVATION | CELL BIOLOGY | Endoplasmic Reticulum - enzymology | Reactive Oxygen Species - metabolism | Humans | NADPH Oxidases - metabolism | Cercopithecus aethiops | Protein Transport - drug effects | Antioxidants - pharmacology | NADPH Oxidase 4 | Mutation - genetics | Protein Tyrosine Phosphatase, Non-Receptor Type 1 - metabolism | Receptor, Epidermal Growth Factor - metabolism | Animals | Substrate Specificity - drug effects | Signal Transduction - drug effects | Endothelial Cells - cytology | Endoplasmic Reticulum - drug effects | Oxidation-Reduction - drug effects | Cell Proliferation - drug effects | Mice | Epidermal Growth Factor - pharmacology | Phosphorylation - drug effects | COS Cells | Endothelial Cells - enzymology | Endothelial Cells - drug effects | Evaluation | Vascular endothelium | Cell research | Cellular signal transduction | Properties | Endoplasmic reticulum
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2. Full Text NADPH oxidase 4 limits bone mass by promoting osteoclastogenesis
by Goettsch, Claudia and Babelova, Andrea and Trummer, Olivia and Erben, Reinhold G and Rauner, Martina and Rammelt, Stefan and Weissmann, Norbert and Weinberger, Valeska and Benkhoff, Sebastian and Kampschulte, Marian and Obermayer-Pietsch, Barbara and Hofbauer, Lorenz C and Brandes, Ralf P and Schröder, Katrin
Journal of Clinical Investigation, ISSN 0021-9738, 11/2013, Volume 123, Issue 11, pp. 4731 - 4738
ROS are implicated in bone diseases. NADPH oxidase 4 (NOX4), a constitutively active enzymatic source of ROS, may contribute to the development of such... 
Reactive Oxygen Species - metabolism | Bone Density - physiology | Humans | Middle Aged | Osteoporosis, Postmenopausal - pathology | Bone Density - genetics | Cell Differentiation - genetics | NADPH Oxidases - deficiency | Bone Resorption - genetics | RANK Ligand - physiology | Monocytes - pathology | NADPH Oxidases - genetics | Female | Osteoclasts - physiology | Monocytes - physiology | Cell Differentiation - physiology | Disease Models, Animal | Bone Resorption - physiopathology | Osteoclasts - pathology | Osteoporosis, Postmenopausal - genetics | NADPH Oxidase 4 | Mice, Knockout | Animals | Bone Resorption - pathology | Osteoporosis, Postmenopausal - physiopathology | Mice | Polymorphism, Single Nucleotide | Macrophage Colony-Stimulating Factor - physiology | NADPH Oxidases - physiology | Oxidases | NADP (Coenzyme) | Physiological aspects | Development and progression | Genetic aspects | Bone diseases | Research | Risk factors | Enzymes | Cell culture | Normal distribution | Colleges & universities | Bones | Bone density
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3. Full Text NADPH Oxidase 4 promotes endothelial angiogenesis through endothelial nitric oxide synthase activation
by Craige, Siobhan M and Chen, Kai and Pei, Yongmei and Li, Chunying and Huang, Xiaoyun and Chen, Christine and Shibata, Rei and Sato, Kaori and Walsh, Kenneth and Keaney, John F
Circulation, ISSN 0009-7322, 08/2011, Volume 124, Issue 6, pp. 731 - 740
Background-Reactive oxygen species serve signaling functions in the vasculature, and hypoxia has been associated with increased reactive oxygen species... 
endothelium | NADPH oxidase 4 | eNOS | angiogenesis | reactive oxygen species | CELLS | OXIDATIVE STRESS | CARDIAC & CARDIOVASCULAR SYSTEMS | SIGNAL-TRANSDUCTION | NAD(P)H OXIDASE | CARDIOVASCULAR-DISEASE | NOX4 | PERIPHERAL VASCULAR DISEASE | HYDROGEN-PEROXIDE | AKT-DEPENDENT PHOSPHORYLATION | GROWTH-FACTOR | PROTEIN-TYROSINE-PHOSPHATASE | Genetic Therapy | Reactive Oxygen Species | Genetic Vectors - administration & dosage | Humans | Recombinant Fusion Proteins - physiology | Genetic Vectors - therapeutic use | Nitric Oxide Synthase Type III - deficiency | RNA Interference | Cattle | NADPH Oxidases - genetics | Nitric Oxide Synthase Type III - physiology | NADPH Oxidases - biosynthesis | Nitric Oxide Synthase Type III - metabolism | RNA, Small Interfering - pharmacology | Enzyme Induction | Ischemia - therapy | Mice, Transgenic | NADPH Oxidase 4 | Nitric Oxide Synthase Type III - genetics | Cells, Cultured - enzymology | Neovascularization, Physiologic - physiology | Animals | Cyclic GMP - metabolism | Hindlimb - blood supply | Mice | Cell Hypoxia - genetics | Endothelial Cells - enzymology | NADPH Oxidases - physiology | Physiological aspects | Hypoxia | Reactive oxygen species | Research | Neovascularization | NADP (Coenzyme)
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4. Full Text NADPH oxidase 4 regulates vascular inflammation in aging and atherosclerosis
by Lozhkin, Andrey and Vendrov, Aleksandr E and Pan, Hua and Wickline, Samuel A and Madamanchi, Nageswara R and Runge, Marschall S
Journal of Molecular and Cellular Cardiology, ISSN 0022-2828, 2016, Volume 102, pp. 10 - 21
Abstract We recently reported that increased NADPH oxidase 4 (NOX4) expression and activity during aging results in enhanced cellular and mitochondrial... 
Cardiovascular | Nanoparticles | Reactive oxygen species | Inflammation | Cytokines | Atherosclerosis | MITOCHONDRIAL OXIDATIVE STRESS | CARDIAC & CARDIOVASCULAR SYSTEMS | MELITTIN-DERIVED PEPTIDES | TGF-BETA | MONOCYTE CHEMOATTRACTANT PROTEIN-1 | CELL BIOLOGY | GROWTH-FACTOR-BETA | SIRNA TRANSFECTION | SMOOTH-MUSCLE-CELLS | NF-KAPPA-B | TRANSCRIPTIONAL REGULATION | CORONARY-ARTERY-DISEASE | Carotid Arteries - metabolism | RNA, Small Interfering - genetics | Vasculitis - metabolism | Reactive Oxygen Species - metabolism | Muscle, Smooth, Vascular - metabolism | Atherosclerosis - genetics | Humans | Vasculitis - etiology | Vasculitis - pathology | NADPH Oxidases - metabolism | Cell Survival - genetics | Male | NF-kappa B - metabolism | Gene Knockdown Techniques | Aging - genetics | RNA Interference | Inflammation Mediators - metabolism | NADPH Oxidases - genetics | Cytokines - genetics | Myocytes, Smooth Muscle - metabolism | Disease Models, Animal | Atherosclerosis - pathology | Cytokines - metabolism | MAP Kinase Kinase Kinases - metabolism | Mitochondria - metabolism | NADPH Oxidase 4 | Atherosclerosis - metabolism | Hydrogen Peroxide - metabolism | Mice, Knockout | Animals | Biomarkers | Carotid Arteries - pathology | Mice | Aging - metabolism | Oxidases | RNA | Genes | Transforming growth factors | Gene expression | Medical colleges | Anopheles | Peptides | Peroxides | Index Medicus
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5. Full Text NADPH oxidase 4 (Nox4) is a major source of oxidative stress in the failing heart
by Junya Kuroda and Tetsuro Ago and Shouji Matsushima and Peiyong Zhai and Michael D. Schneider and Junichi Sadoshima and Salvador Moncada
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 8/2010, Volume 107, Issue 35, pp. 15565 - 15570
NAD(P)H oxidases (Noxs) produce O 2 − and play an important role in cardiovascular pathophysiology. The Nox4 isoform is expressed primarily in the mitochondria... 
Heart | Oxidases | Oxidative stress | Cardiomegaly | Up regulation | Mitochondria | Transcriptional regulatory elements | Reactive oxygen species | Fibrosis | Apoptosis | Cardiac hypertrophy | Superoxide | NAD(P)H oxidase | MYOCARDIUM | PRESSURE-OVERLOAD | MYOCYTES | mitochondria | MULTIDISCIPLINARY SCIENCES | FAILURE | MITOCHONDRIAL PERMEABILITY TRANSITION | CARDIAC-HYPERTROPHY | RADICALS | cardiac hypertrophy | superoxide | REVEALS | Reactive Oxygen Species - metabolism | Oxidative Stress | NADPH Oxidases - metabolism | Immunoblotting | Male | Isoenzymes - metabolism | Myocardium - metabolism | NADPH Oxidases - genetics | Female | Heart - physiopathology | In Situ Nick-End Labeling | Echocardiography | Isoenzymes - genetics | Mice, Inbred C57BL | Cardiomegaly - physiopathology | Heart Failure - genetics | Myocardium - pathology | Heart Failure - metabolism | Mitochondria - metabolism | Heart Failure - pathology | NADPH Oxidase 4 | Reverse Transcriptase Polymerase Chain Reaction | Mice, Knockout | Myocytes, Cardiac - pathology | Animals | Myocytes, Cardiac - metabolism | Mice | Cardiomegaly - genetics | Mitochondria - physiology | Cardiomegaly - metabolism | Heart failure | Composition | Genetic aspects | Health aspects | Biological Sciences
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6. Full Text NADPH oxidase 4 is an oncoprotein localized to mitochondria
by Graham, Kelly A and Kulawiec, Mariola and Owens, Kjerstin M and Li, Xiurong and Desouki, Mohamed M and Chandra, Dhyan and Singh, Keshav K
Cancer Biology & Therapy, ISSN 1538-4047, 08/2010, Volume 10, Issue 3, pp. 223 - 231
  Reactive oxygen species (ROS) are known to be involved in many physiological and pathological processes. Initially ROS-producing NADPH oxidase (NOX) proteins... 
Binding | Proteins | Landes | Calcium | Bioscience | Biology | Cell | Cycle | Cancer | Organogenesis | NADPH oxidase 4 | Oncogenesis | Breast cancer | Catalase | ACTIVATION | breast cancer | CANCER | CROSS-TALK | RESPONSES | NAD(P)H OXIDASE | SMOOTH-MUSCLE | ONCOLOGY | oncogenesis | ENDOTHELIAL-CELLS | NOX4 | HYDROGEN-PEROXIDE | TUMORIGENESIS | catalase | Mitochondria - enzymology | NIH 3T3 Cells | Reactive Oxygen Species - metabolism | Humans | Gene Expression Regulation, Neoplastic | NADPH Oxidases - metabolism | NADPH Oxidase 4 | Ovarian Neoplasms - enzymology | Hydrogen Peroxide - metabolism | Breast Neoplasms - enzymology | Animals | Breast Neoplasms - genetics | Transfection | Mitochondria - genetics | Breast Neoplasms - pathology | Cell Line, Tumor | NADPH Oxidases - genetics | Female | Mice | Apoptosis - physiology | NADPH Oxidases - biosynthesis | Research Paper
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7. Full Text NADPH oxidase 4 protects against development of endothelial dysfunction and atherosclerosis in LDL receptor deficient mice
by Langbein, Heike and Brunssen, Coy and Hofmann, Anja and Cimalla, Peter and Brux, Melanie and Bornstein, Stefan R and Deussen, Andreas and Koch, Edmund and Morawietz, Henning
European Heart Journal, ISSN 0195-668X, 06/2016, Volume 37, Issue 22, pp. 1753 - 1761
Aims Endothelial dysfunction is an early step in the development of atherosclerosis. Increased formation of superoxide anions by NADPH oxidase Nox1, 2, and 5... 
Endothelial dysfunction | Nox4 | NADPH oxidase 4 | Flow-mediated dilation | Atherosclerosis | Ldlr2/2 mice | OXIDATIVE STRESS | ACTIVATION | CARDIAC & CARDIOVASCULAR SYSTEMS | SUPEROXIDE-PRODUCTION | SYNTHASE | INHIBITION | NOX FAMILY | ROS | NITRIC-OXIDE | HYDROGEN-PEROXIDE | VASODILATATION | Ldlr(-/-) mice | NADPH Oxidases | Animals | Endothelial Cells | Hydrogen Peroxide | Mice, Inbred C57BL | Receptors, LDL | Mice | NADPH Oxidase 4 | Mice, Knockout | Basic Science | Ldlr | mice
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8. Full Text Endothelial NADPH oxidase 4 protects ApoE-/- mice from atherosclerotic lesions
by Craige, Siobhan M and Kant, Shashi and Reif, Michaella and Chen, Kai and Pei, Yongmei and Angoff, Rebecca and Sugamura, Koichi and Fitzgibbons, Timothy and Keaney, John F
Free Radical Biology and Medicine, ISSN 0891-5849, 12/2015, Volume 89, pp. 1 - 7
Vascular reactive oxygen species (ROS) are known to be involved in atherosclerosis development and progression. NADPH oxidase 4 (Nox4) is a constitutively... 
Reactive oxygen species | CXCL9 | NADPH Oxidase 4 | T regulatory cells | Atherosclerosis | LOCALIZATION | OXIDATIVE STRESS | ACTIVATION | SUPEROXIDE | BIOCHEMISTRY & MOLECULAR BIOLOGY | HYPERCHOLESTEROLEMIA | INDUCTION | RESPONSES | ENDOCRINOLOGY & METABOLISM | REGULATORY T-CELLS | NOX4 | REVEALS | Endothelium, Vascular - cytology | T-Lymphocytes, Regulatory - metabolism | Cell Proliferation | Reactive Oxygen Species - metabolism | Oxidative Stress | Atherosclerosis - genetics | Humans | NADPH Oxidases - metabolism | Male | Aorta - metabolism | Interferon-gamma - metabolism | Immunoenzyme Techniques | NADPH Oxidases - genetics | Female | Real-Time Polymerase Chain Reaction | Cytokines - blood | Atherosclerosis - pathology | Mice, Inbred C57BL | RNA, Messenger - genetics | Cells, Cultured | Mice, Transgenic | Reverse Transcriptase Polymerase Chain Reaction | Atherosclerosis - metabolism | Blotting, Western | Mice, Knockout | Animals | Endothelium, Vascular - metabolism | Apolipoproteins E - physiology | Mice | Aorta - cytology | Atherosclerosis - prevention & control | Oxidases | Genetic engineering | Biological response modifiers | T cells | Apolipoproteins | Cells | Cardiovascular agents | Interferon gamma | Endothelium | Proteins | atherosclerosis | reactive oxygen species
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9. Full Text Inhibition of reactive oxygen species by lovastatin downregulates vascular endothelial growth factor expression and ameliorates blood-retinal barrier breakdown in db/db mice: Role of NADPH oxidase 4
by Li, Jingming and Wang, Joshua J and Yu, Qiang and Chen, Kai and Mahadev, Kalyankar and Zhang, Sarah X
Diabetes, ISSN 0012-1797, 06/2010, Volume 59, Issue 6, pp. 1528 - 1538
OBJECTIVE-Oxidative stress is a key pathogenic factor in diabetic retinopathy. We previously showed that lovastatin mitigates blood-retinal barrier (BRB)... 
SIGNAL-TRANSDUCTION | CELLS | LOCALIZATION | NAD(P)H OXIDASE | OXIDATIVE STRESS | PROLIFERATIVE DIABETIC-RETINOPATHY | MACULAR EDEMA | INFLAMMATION | ENDOCRINOLOGY & METABOLISM | NOX4 | ENDOPLASMIC-RETICULUM STRESS | Endothelium, Vascular - cytology | Blood-Retinal Barrier - physiology | Reactive Oxygen Species - metabolism | Lovastatin - pharmacology | Oxidative Stress - physiology | NADPH Oxidases - metabolism | Capillaries - drug effects | Endothelium, Vascular - drug effects | NADPH Oxidase 4 | Down-Regulation - drug effects | Enzyme Activation - drug effects | Vascular Endothelial Growth Factor A - genetics | Blood-Retinal Barrier - drug effects | Endothelium, Vascular - physiology | Capillaries - physiology | Retina - physiology | Animals | Capillaries - cytology | Cattle | NADPH Oxidases - drug effects | NADPH Oxidases - genetics | Mice | Oxidative Stress - drug effects | Diabetic retinopathy | Active oxygen | Physiological aspects | Lovastatin | Genetic aspects | Dosage and administration | Research | Drug therapy | Vascular endothelial growth factor | Health aspects | Risk factors | Original
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10. Full Text NADPH Oxidase 4 Is Expressed in Pulmonary Artery Adventitia and Contributes to Hypertensive Vascular Remodeling
by Barman, Scott A and Chen, Feng and Su, Yunchao and Dimitropoulou, Christiana and Wang, Yusi and Catravas, John D and Han, Weihong and Orfi, Laszlo and Szantai-Kis, Csaba and Keri, Gyorgy and Szabadkai, Istvan and Barabutis, Nektarios and Rafikova, Olga and Rafikov, Ruslan and Black, Stephen M and Jonigk, Danny and Giannis, Athanassios and Asmis, Reto and Stepp, David W and Ramesh, Ganesan and Fulton, David J.R
Arteriosclerosis, Thrombosis, and Vascular Biology, ISSN 1079-5642, 08/2014, Volume 34, Issue 8, pp. 1704 - 1715
OBJECTIVE—Pulmonary hypertension (PH) is a progressive disease arising from remodeling and narrowing of pulmonary arteries (PAs) resulting in high pulmonary... 
Adventitia | Fibroblast | NADPH oxidase | Pulmonary artery | pulmonary artery | ACTIVATION | adventitia | PROLIFERATION | FIBROBLASTS | NAD(P)H OXIDASE | fibroblast | CHRONIC HYPOXIA | MODELS | INFLAMMATION | NOX4 | PERIPHERAL VASCULAR DISEASE | SMOOTH-MUSCLE-CELLS | HEMATOLOGY | MOLECULAR-MECHANISMS | Up-Regulation | Antihypertensive Agents - pharmacology | Fibroblasts - enzymology | Cell Proliferation | Reactive Oxygen Species - metabolism | Humans | Monocrotaline | NADPH Oxidases - metabolism | Pyrroles | Extracellular Matrix - metabolism | Male | Dose-Response Relationship, Drug | Extracellular Matrix - genetics | Transfection | Time Factors | HEK293 Cells | Adventitia - enzymology | NADPH Oxidases - genetics | Hypertrophy, Right Ventricular - pathology | Hypertension, Pulmonary - drug therapy | Indoles | Hypertension, Pulmonary - enzymology | Disease Models, Animal | Signal Transduction | Mice, Inbred C57BL | NADPH Oxidases - antagonists & inhibitors | Enzyme Inhibitors - pharmacology | Rats | Familial Primary Pulmonary Hypertension | Hypertension, Pulmonary - genetics | Hypoxia - complications | Adventitia - drug effects | NADPH Oxidase 4 | Pulmonary Artery - drug effects | Fibroblasts - pathology | Hypertrophy, Right Ventricular - enzymology | Rats, Sprague-Dawley | Pulmonary Artery - enzymology | Animals | Hypertrophy, Right Ventricular - prevention & control | Adventitia - pathology | Mice | Hypertension, Pulmonary - etiology | Hypertension, Pulmonary - pathology | Pulmonary Artery - pathology | Cell Movement | Index Medicus
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11. Full Text Small-molecule inhibitors of NADPH oxidase 4
by Borbély, Gábor and Szabadkai, István and Horváth, Zoltán and Markó, Péter and Varga, Zoltán and Breza, Nóra and Baska, Ferenc and Vántus, Tibor and Huszár, Mónika and Geiszt, Miklós and Hunyady, László and Buday, László and Örfi, László and Kéri, György
Journal of Medicinal Chemistry, ISSN 0022-2623, 09/2010, Volume 53, Issue 18, pp. 6758 - 6762
NOX enzymes are the major contributors in many oxidative damage related diseases. Unfortunately, at present no specific NOX inhibitor is available. Here, we... 
TYROSINE KINASE INHIBITORS | CELLS | APIGENIN | CHEMISTRY, MEDICINAL | PROTEIN-KINASE | DISEASE | Cell Line | Oxalates - chemistry | Aminosalicylic Acids - pharmacology | Humans | NADPH Oxidases - antagonists & inhibitors | Models, Molecular | Structure-Activity Relationship | NADPH Oxidase 4 | Pyrimidines - pharmacology | Pyrimidines - chemistry | Hydrogen Peroxide - metabolism | Phenanthrenes - pharmacology | Phenanthrenes - chemical synthesis | Aminosalicylic Acids - chemistry | Indoles - pharmacology | Flavonoids - pharmacology | Flavonoids - chemistry | Indoles - chemistry | Oxalates - pharmacology
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12. Full Text Metabolomics reveals a key role for fumarate in mediating the effects of NADPH oxidase 4 in diabetic kidney disease
by You, Young-Hyun and Quach, Tammy and Saito, Rintaro and Pham, Jessica and Sharma, Kumar
Journal of the American Society of Nephrology, ISSN 1046-6673, 02/2016, Volume 27, Issue 2, pp. 466 - 481
The NADPH oxidase (NOX) isoform NOX4 has been linked with diabetic kidney disease (DKD). However, a mechanistic understanding of the downstream effects of NOX4... 
NAD(P)H OXIDASE | UTERINE LEIOMYOMATOSIS | HYDRATASE DEFICIENCY | DB/DB MICE | TCA CYCLE | UROLOGY & NEPHROLOGY | HEREDITARY LEIOMYOMATOSIS | NOX4 | ENDOPLASMIC-RETICULUM STRESS | HYPOXIA | RENAL-CELL CANCER | Metabolomics | Animals | Diabetic Nephropathies - metabolism | Fumarate Hydratase - physiology | Mice, Inbred C57BL | Male | Mice | NADPH Oxidase 4 | NADPH Oxidases - physiology | NADPH oxidase | mitochondria | reactive oxygen species | podocyte | fibrosis | diabetic nephropathy | Basic Research
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13. Full Text NADPH Oxidase 4 Induces Cardiac Fibrosis and Hypertrophy Through Activating Akt/mTOR and NFκB Signaling Pathways
by Zhao, Qingwei David and Viswanadhapalli, Suryavathi and Williams, Paul and Shi, Qian and Tan, Chunyan and Yi, Xiaolan and Bhandari, Basant and Abboud, Hanna E
Circulation, ISSN 0009-7322, 02/2015, Volume 131, Issue 7, pp. 643 - 655
BACKGROUND—NADPH oxidase 4 (Nox4) has been implicated in cardiac remodeling, but its precise role in cardiac injury remains controversial. Furthermore, little... 
MTORC1 | Reactive oxygen species | NFκB | NADPH oxidase | Fibrosis | Hypertrophy | TRANSCRIPTION FACTORS | OXIDATIVE STRESS | CARDIAC & CARDIOVASCULAR SYSTEMS | hypertrophy | ANGIOTENSIN-II | reactive oxygen species | IN-VIVO | TUBULAR EPITHELIAL-CELLS | GENE-EXPRESSION | PERIPHERAL VASCULAR DISEASE | fibrosis | RAT-HEART | mTORC1 | UP-REGULATION | NF kappa B | ENDOTHELIAL GROWTH-FACTOR | PROMOTES APOPTOSIS | TOR Serine-Threonine Kinases - metabolism | Humans | Mice, Inbred C57BL | Cardiomegaly - pathology | Male | Mice, Transgenic | NF-kappa B - metabolism | NADPH Oxidase 4 | Fibrosis - metabolism | Animals | Signal Transduction - physiology | Mice | Fibrosis - pathology | NADPH Oxidases - biosynthesis | Proto-Oncogene Proteins c-akt - metabolism | Cardiomegaly - metabolism | signaling pathways
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14. Full Text Naringin ameliorates diabetic nephropathy by inhibiting NADPH oxidase 4
by Zhang, Junwei and Yang, Suxia and Li, Huicong and Chen, Fang and Shi, Jun
European Journal of Pharmacology, ISSN 0014-2999, 06/2017, Volume 804, pp. 1 - 6
Naringin, a naturally flavanone glycoside, has been previously demonstrated to alleviate diabetic kidney disease by inhibiting oxidative stress and... 
Oxidative stress | Diabetic nephropathy | NOX4 | Reactive oxygen species | Naringin | INJURY | PHARMACOLOGY & PHARMACY | MECHANISMS | PODOCYTE DEPLETION | DELETION | Gene Expression Regulation, Enzymologic - drug effects |