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1. Full Text Endothelial NADPH Oxidase-2 Promotes Interstitial Cardiac Fibrosis and Diastolic Dysfunction Through Proinflammatory Effects and Endothelial-Mesenchymal Transition
by Murdoch, Colin E., PhD and Chaubey, Sanjay, MBBCh, PhD and Zeng, Lingfang, PhD and Yu, Bin, PhD and Ivetic, Aleksander, PhD and Walker, Simon J., BSc and Vanhoutte, Davy, PhD and Heymans, Stephane, MD, PhD and Grieve, David J., PhD and Cave, Alison C., PhD and Brewer, Alison C., PhD and Zhang, Min, MD, PhD and Shah, Ajay M., MD, FMedSci
Journal of the American College of Cardiology, ISSN 0735-1097, 06/2014, Volume 63, Issue 24, pp. 2734 - 2741
Cardiovascular | Internal Medicine | endothelial-mesenchymal transition | diastolic dysfunction | endothelium | NADPH (nicotinamide adenine dinucleotide phosphate) oxidase | angiotensin II | Cardiac & Cardiovascular Systems | Life Sciences & Biomedicine | Cardiovascular System & Cardiology | Science & Technology | Cardiology. Vascular system | Heart | Biological and medical sciences | Medical sciences | Heart Failure, Diastolic - genetics | Mesenchymal Stromal Cells - enzymology | Humans | Cardiomegaly - pathology | Male | Endothelium, Vascular - enzymology | Membrane Glycoproteins - physiology | Ventricular Dysfunction, Left - genetics | Ventricular Dysfunction, Left - pathology | NADPH Oxidases - genetics | Ventricular Dysfunction, Left - enzymology | Inflammation Mediators - physiology | Fibrosis - genetics | Fibrosis - enzymology | Cells, Cultured | Heart Failure, Diastolic - enzymology | Mice, Transgenic | Cardiomegaly - enzymology | Heart Failure, Diastolic - pathology | NADPH Oxidase 2 | Membrane Glycoproteins - genetics | Animals | Endothelium, Vascular - pathology | Mice | Fibrosis - pathology | Mesenchymal Stromal Cells - pathology | Cardiomegaly - genetics | NADPH Oxidases - physiology | Oxidases | Fibrosis | Stem cells | Endothelium | Hypertension | Heart failure | Genotype & phenotype | Stroke | Heart attacks | Pathogenesis | Rodents | Cardiomyocytes | Variance analysis | Index Medicus | Abridged Index Medicus
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2. Full Text Upregulation of Nox4 by Hypertrophic Stimuli Promotes Apoptosis and Mitochondrial Dysfunction in Cardiac Myocytes
by Ago, Tetsuro and Kuroda, Junya and Pain, Jayashree and Fu, Cexiong and Li, Hong and Sadoshima, Junichi
Circulation research, ISSN 0009-7330, 04/2010, Volume 106, Issue 7, pp. 1253 - 1264
Aging | Oxidative stress | Reactive oxygen species | Superoxide | Apoptosis | Hypertrophy | Cardiac & Cardiovascular Systems | Peripheral Vascular Disease | Life Sciences & Biomedicine | Hematology | Cardiovascular System & Cardiology | Science & Technology | Aconitate Hydratase - metabolism | Up-Regulation | Cysteine | Cell Proliferation | Uncoupling Agents - pharmacology | Oxidative Stress | Rats, Wistar | Ventricular Function, Left | Apoptosis - drug effects | Mitochondria, Heart - pathology | Humans | NADPH Oxidases - metabolism | Cardiomegaly - pathology | Mitochondria, Heart - drug effects | Myocytes, Cardiac - enzymology | Transfection | Ventricular Dysfunction, Left - genetics | Rotenone - pharmacology | Superoxides - metabolism | Ventricular Dysfunction, Left - pathology | NADPH Oxidases - genetics | Ventricular Dysfunction, Left - enzymology | Disease Models, Animal | Oxidation-Reduction | NADPH Oxidases - antagonists & inhibitors | Cells, Cultured | Enzyme Inhibitors - pharmacology | Mitochondria, Heart - enzymology | Cardiomegaly - physiopathology | Rats | Genotype | Mice, Transgenic | Cardiomegaly - enzymology | NADPH Oxidase 4 | Onium Compounds - pharmacology | NADH Dehydrogenase - metabolism | Ventricular Dysfunction, Left - physiopathology | Aging - pathology | Myocytes, Cardiac - pathology | Phenotype | Animals | Myocytes, Cardiac - drug effects | Fibrosis | Mice | Cardiomegaly - genetics | Aging - metabolism | Index Medicus | apoptosis | aging | superoxide | hypertrophy | oxidative stress
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3. Full Text Matrix Metalloproteinase-28 Deletion Exacerbates Cardiac Dysfunction and Rupture After Myocardial Infarction in Mice by Inhibiting M2 Macrophage Activation
by Ma, Yonggang and Halade, Ganesh V and Zhang, Jianhua and Ramirez, Trevi A and Levin, Daniel and Voorhees, Andrew and Jin, Yu-Fang and Han, Hai-Chao and Manicone, Anne M and Lindsey, Merry L
Circulation research, ISSN 0009-7330, 02/2013, Volume 112, Issue 4, pp. 675 - 688
fibroblast | MMP-28 | inflammation | macrophage phenotype | myocardial infarction | Cardiac & Cardiovascular Systems | Peripheral Vascular Disease | Life Sciences & Biomedicine | Hematology | Cardiovascular System & Cardiology | Science & Technology | Myocardial Infarction - blood | Cell Adhesion Molecules - genetics | Cicatrix - etiology | Extracellular Matrix Proteins - biosynthesis | Male | Matrix Metalloproteinases, Secreted - deficiency | Pulmonary Edema - etiology | Myocytes, Cardiac - enzymology | Myofibroblasts - metabolism | Ventricular Dysfunction, Left - enzymology | Ventricular Remodeling - genetics | Female | Myocardial Infarction - physiopathology | Transcription, Genetic | Cytokines - genetics | Heart Rupture - enzymology | Receptors, Cytokine - genetics | Matrix Metalloproteinase 9 - blood | Myocardial Infarction - enzymology | Macrophage Activation - physiology | Macrophages - classification | Cell Adhesion Molecules - biosynthesis | Receptors, Cytokine - biosynthesis | Extracellular Matrix Proteins - genetics | Mice, Inbred C57BL | Gene Expression Regulation | Ventricular Dysfunction, Left - etiology | Inflammation | Ventricular Remodeling - physiology | Macrophages - enzymology | Mice, Knockout | Collagen - metabolism | Myocardial Infarction - complications | Heart Rupture - etiology | Animals | Pulmonary Edema - enzymology | Matrix Metalloproteinases, Secreted - genetics | Matrix Metalloproteinases, Secreted - physiology | Protein-Lysine 6-Oxidase - metabolism | Cicatrix - enzymology | Mice | Cytokines - biosynthesis | Index Medicus
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4. Full Text p53-PGC-1α Pathway Mediates Oxidative Mitochondrial Damage and Cardiomyocyte Necrosis Induced by Monoamine Oxidase-A Upregulation: Role in Chronic Left Ventricular Dysfunction in Mice
by Villeneuve, Christelle and Guilbeau-Frugier, Céline and Sicard, Pierre and Lairez, Olivier and Ordener, Catherine and Duparc, Thibaut and De Paulis, Damien and Couderc, Bettina and Spreux-Varoquaux, Odile and Tortosa, Florence and Garnier, Anne and Knauf, Claude and Valet, Philippe and Borchi, Elisabetta and Nediani, Chiara and Gharib, Abdallah and Ovize, Michel and Delisle, Marie-Bernadette and Parini, Angelo and Mialet-Perez, Jeanne
Antioxidants & redox signaling, ISSN 1523-0864, 01/2013, Volume 18, Issue 1, pp. 5 - 18
Original Research Communications | Biochemistry & Molecular Biology | Endocrinology & Metabolism | Life Sciences & Biomedicine | Science & Technology | Up-Regulation | Hypertrophy, Left Ventricular - enzymology | Oxidative Stress | Cardiomyopathy, Dilated - enzymology | Male | Monoamine Oxidase - genetics | Heart Ventricles - enzymology | Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha | Ventricular Dysfunction, Left - pathology | Ventricular Dysfunction, Left - enzymology | Heart Ventricles - pathology | Oxidation-Reduction | Mice, Inbred C57BL | Cells, Cultured | Mitochondria, Heart - enzymology | Tumor Suppressor Protein p53 - metabolism | Enzyme Induction | Rats | Mice, Transgenic | Rats, Sprague-Dawley | Myocytes, Cardiac - pathology | Animals | Fibrosis | Myocytes, Cardiac - metabolism | Trans-Activators - metabolism | Mice | Transcription Factors | Chronic Disease | Necrosis - enzymology | Monoamine Oxidase - metabolism | Index Medicus | Life Sciences | Cellular Biology
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5. Full Text Myocardial overexpression of TIMP3 after myocardial infarction exerts beneficial effects by promoting angiogenesis and suppressing early proteolysis
by Takawale, Abhijit and Zhang, Pu and Azad, Abul and Wang, Wang and Wang, Xiuhua and Murray, Allan G and Kassiri, Zamaneh
American journal of physiology. Heart and circulatory physiology, ISSN 0363-6135, 2017, Volume 313, Issue 2, pp. H224 - H236
Remodeling | Tissue inhibitor of metalloproteinases 3 | Cardiac & Cardiovascular Systems | Physiology | Peripheral Vascular Disease | Life Sciences & Biomedicine | Cardiovascular System & Cardiology | Science & Technology | Myocardial Infarction - genetics | Up-Regulation | Cell Proliferation | Hypertrophy, Left Ventricular - enzymology | Ventricular Function, Left | Coronary Vessels - physiopathology | Humans | Male | Recovery of Function | Myocardial Infarction - therapy | Ventricular Remodeling | Hypertrophy, Left Ventricular - genetics | Time Factors | Ventricular Dysfunction, Left - genetics | Proteolysis | Tissue Inhibitor of Metalloproteinase-3 - biosynthesis | Adenoviridae - genetics | Ventricular Dysfunction, Left - enzymology | Myocardial Infarction - physiopathology | Disease Models, Animal | Myocardial Infarction - enzymology | Tissue Inhibitor of Metalloproteinase-3 - genetics | Coronary Vessels - enzymology | Transduction, Genetic | Signal Transduction | Hypertrophy, Left Ventricular - prevention & control | Mice, Inbred C57BL | Myocardium - pathology | Ventricular Dysfunction, Left - physiopathology | Ventricular Dysfunction, Left - prevention & control | Myocardium - enzymology | Animals | Adenoviridae - metabolism | Hypertrophy, Left Ventricular - physiopathology | Matrix Metalloproteinases - metabolism | Endothelial Cells - pathology | Genetic Vectors | Endothelial Cells - enzymology | Neovascularization, Physiologic | Genetic Therapy - methods | Myocardial infarction | Regulators | Heart attacks | Echocardiography | Matrix metalloproteinases | Coronary artery | Effects | Density | Endothelial cells | Arteries | Angiogenesis | Matrix | Antiangiogenics | Rodents | Dilation | Protein expression | Disruption | Index Medicus
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6. Full Text Cardiomyocyte dimethylarginine dimethylaminohydrolase-1 (DDAH1) plays an important role in attenuating ventricular hypertrophy and dysfunction
by Xu, Xin and Zhang, Ping and Kwak, Dongmin and Fassett, John and Yue, Wenhui and Atzler, Dorothee and Hu, Xinli and Liu, Xiaohong and Wang, Huan and Lu, Zhongbing and Guo, Haipeng and Schwedhelm, Edzard and Böger, Rainer H and Chen, Peijie and Chen, Yingjie
Basic research in cardiology, ISSN 0300-8428, 9/2017, Volume 112, Issue 5, pp. 1 - 11
ADMA | Medicine & Public Health | Cardiology | Nitric oxide | Ventricular hypertrophy | Cardiac & Cardiovascular Systems | Life Sciences & Biomedicine | Cardiovascular System & Cardiology | Science & Technology | Hypertrophy, Left Ventricular - enzymology | Ventricular Function, Left | Male | Tyrosine - analogs & derivatives | Arginine - analogs & derivatives | Myocytes, Cardiac - enzymology | Ventricular Remodeling | Hypertrophy, Left Ventricular - genetics | Ventricular Dysfunction, Left - genetics | Ventricular Dysfunction, Left - enzymology | Amidohydrolases - deficiency | Disease Models, Animal | Amidohydrolases - metabolism | Genetic Predisposition to Disease | Atrial Natriuretic Factor - metabolism | Signal Transduction | Amidohydrolases - genetics | Hypertrophy, Left Ventricular - prevention & control | Ventricular Dysfunction, Left - physiopathology | Ventricular Dysfunction, Left - prevention & control | Mice, Knockout | Myocytes, Cardiac - pathology | Phenotype | Tyrosine - metabolism | Animals | Arginine - blood | Fibrosis | Hypertrophy, Left Ventricular - physiopathology | Nitric Oxide - metabolism | Heart | Physiological aspects | Heart enlargement | Analysis | Exercise therapy | Sarcolemma | Stresses | Homeostasis | Cardiomyocytes | Bioavailability | Endothelial cells | Eutrophication | Degradation | Rodents | Aging | Aorta | Mice | Nitrotyrosine | Ventricle | Heart diseases | Dimethylargininase | Hypertrophy | Plasmas (physics) | Index Medicus
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7. Full Text TNF-α down-regulates sarcoplasmic reticulum Ca2+ ATPase expression and leads to left ventricular diastolic dysfunction through binding of NF-κB to promoter response element
by Tsai, Chia-Ti and Wu, Cho-Kai and Lee, Jen-Kuang and Chang, Sheng-Nan and Kuo, Yu-Min and Wang, Yi-Chih and Lai, Ling-Ping and Chiang, Fu-Tien and Hwang, Juey-Jen and Lin, Jiunn-Lee
Cardiovascular research, ISSN 0008-6363, 2015, Volume 105, Issue 3, pp. 318 - 329
Diastolic dysfunction | SERCA2a | TNF-α | Transcription | Simvastatin | Atp2a2 | Cardiac & Cardiovascular Systems | Life Sciences & Biomedicine | Cardiovascular System & Cardiology | Science & Technology | Inflammation - chemically induced | Tumor Necrosis Factor-alpha - metabolism | Diastole | Rats, Wistar | Male | NF-kappa B - metabolism | Ventricular Dysfunction, Left - chemically induced | Lipopolysaccharides | Dose-Response Relationship, Drug | Myocytes, Cardiac - enzymology | Ventricular Dysfunction, Left - genetics | Ventricular Dysfunction, Left - enzymology | Transcription, Genetic | Binding Sites | Disease Models, Animal | Cell Line | Promoter Regions, Genetic | NF-kappa B - antagonists & inhibitors | Sarcoplasmic Reticulum Calcium-Transporting ATPases - metabolism | Signal Transduction | Anti-Inflammatory Agents - pharmacology | Down-Regulation | Ventricular Function, Left - drug effects | Ventricular Dysfunction, Left - physiopathology | Ventricular Dysfunction, Left - prevention & control | Gene Expression Regulation, Enzymologic | Tumor Necrosis Factor-alpha - pharmacology | Animals | Myocytes, Cardiac - drug effects | NF-kappa B - genetics | Inflammation - genetics | Protein Binding | Inflammation - prevention & control | Mice | Sarcoplasmic Reticulum Calcium-Transporting ATPases - genetics | Inflammation - enzymology | Inflammation - physiopathology | Index Medicus
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8. Full Text Decreased creatine kinase is linked to diastolic dysfunction in rats with right heart failure induced by pulmonary artery hypertension
by Fowler, Ewan D and Benoist, David and Drinkhill, Mark J and Stones, Rachel and Helmes, Michiel and Wüst, Rob C.I and Stienen, Ger J.M and Steele, Derek S and White, Ed
Journal of molecular and cellular cardiology, ISSN 0022-2828, 2015, Volume 86, pp. 1 - 8
Cardiovascular | Right ventricular failure | Creatine kinase | Diastolic sarcomere length | Monocrotaline | Pulmonary artery hypertension | Cardiac & Cardiovascular Systems | Life Sciences & Biomedicine | Cardiovascular System & Cardiology | Science & Technology | Cell Biology | Diastole | Calcium - metabolism | Heart Failure - enzymology | Humans | Rats | Myocardium - pathology | Heart Failure - pathology | Ventricular Dysfunction, Right - enzymology | Pulmonary Artery - enzymology | Sarcomeres - pathology | Myocytes, Cardiac - enzymology | Myocytes, Cardiac - pathology | Myocardium - enzymology | Animals | Creatine Kinase - biosynthesis | Adenosine Triphosphate - metabolism | Creatine Kinase - metabolism | Sarcomeres - enzymology | Hypertension, Pulmonary - pathology | Hypertension, Pulmonary - enzymology | Pulmonary Artery - pathology | Ventricular Dysfunction, Right - pathology | Heart failure | Hypertension | Index Medicus | Original
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9. Full Text Matrix metalloproteinase-9 deletion attenuates myocardial fibrosis and diastolic dysfunction in ageing mice
by Chiao, Ying Ann and Ramirez, Trevi A and Zamilpa, Rogelio and Okoronkwo, S. Michelle and Dai, Qiuxia and Zhang, Jianhua and Jin, Yu-Fang and Lindsey, Merry L
Cardiovascular research, ISSN 0008-6363, 12/2012, Volume 96, Issue 3, pp. 444 - 455
Diastolic function | Extracellular matrix | Matrix metalloproteinase | Ageing | Collagen | Cardiac & Cardiovascular Systems | Life Sciences & Biomedicine | Cardiovascular System & Cardiology | Science & Technology | Cardiology. Vascular system | Biological and medical sciences | Medical sciences | Blood Pressure | Cell Adhesion Molecules - genetics | Phosphorylation | Age Factors | Diastole | Ventricular Function, Left | Male | Systole | Ventricular Dysfunction, Left - genetics | Matrix Metalloproteinase 8 - metabolism | Matrix Metalloproteinase 9 - genetics | Smad2 Protein - genetics | Ventricular Dysfunction, Left - pathology | Ventricular Dysfunction, Left - enzymology | Female | Real-Time Polymerase Chain Reaction | Matrix Metalloproteinase 8 - genetics | Signal Transduction | Mice, Inbred C57BL | Gene Expression Regulation | Smad2 Protein - metabolism | Ventricular Dysfunction, Left - etiology | Genotype | Myocardium - pathology | Matrix Metalloproteinase 9 - deficiency | Cell Adhesion Molecules - metabolism | Ventricular Dysfunction, Left - physiopathology | Ventricular Dysfunction, Left - prevention & control | Aging - pathology | Mice, Knockout | Collagen - metabolism | Myocardium - enzymology | Phenotype | Animals | Transforming Growth Factor beta - genetics | Fibrosis | Connective Tissue Growth Factor - genetics | Mice | Transforming Growth Factor beta - metabolism | Connective Tissue Growth Factor - metabolism | Aging - metabolism | Index Medicus | Original
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