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1. 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
RATIONALE:NADPH oxidases are a major source of superoxide (O2) in the cardiovascular system. The function of Nox4, a member of the Nox family of NADPH... 
Aging | Oxidative stress | Reactive oxygen species | Superoxide | Apoptosis | Hypertrophy | CELLS | PRESSURE-OVERLOAD | CARDIAC & CARDIOVASCULAR SYSTEMS | hypertrophy | PHOSPHORYLATION | apoptosis | ANGIOTENSIN-II | FAMILY NADPH OXIDASES | FREE-RADICALS | NAD(P)H OXIDASE | reactive oxygen species | PERIPHERAL VASCULAR DISEASE | GENERATION | aging | superoxide | HEMATOLOGY | oxidative stress | 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
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2. 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
Objectives This study sought to investigate the effect of endothelial dysfunction on the development of cardiac hypertrophy and fibrosis. Background... 
Cardiovascular | Internal Medicine | endothelial-mesenchymal transition | diastolic dysfunction | endothelium | NADPH (nicotinamide adenine dinucleotide phosphate) oxidase | angiotensin II | CELLS | OXIDATIVE STRESS | CARDIAC & CARDIOVASCULAR SYSTEMS | ANGIOGENESIS | HEART-FAILURE | ATHEROSCLEROSIS | ANGIOTENSIN-II | PATHOPHYSIOLOGY | HYPERTROPHY | MICE | CONTRIBUTES | 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 | Heart | 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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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
RATIONALE:Matrix metalloproteinase (MMP)-28 regulates the inflammatory and extracellular matrix responses in cardiac aging, but the roles of MMP-28 after... 
fibroblast | MMP-28 | inflammation | macrophage phenotype | myocardial infarction | LYSYL OXIDASE | CARDIAC & CARDIOVASCULAR SYSTEMS | TGF-BETA | VENTRICULAR-FUNCTION | HEART-FAILURE | CORONARY MICROEMBOLIZATION | REPAIR | MATRIX-METALLOPROTEINASE-9 | PERIPHERAL VASCULAR DISEASE | EPILYSIN MMP-28 | TNF-ALPHA | TARGETED DELETION | HEMATOLOGY | 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
Aims: Oxidative stress and mitochondrial dysfunction participate together in the development of heart failure (HF). mRNA levels of monoamine oxidase-A (MAO-A),... 
Original Research Communications | APOPTOSIS | PRESSURE-OVERLOAD | MAO-A | PGC-1-ALPHA | BIOCHEMISTRY & MOLECULAR BIOLOGY | HEART-FAILURE | ENDOCRINOLOGY & METABOLISM | MESANGIAL CELLS | SEROTONIN | DILATED CARDIOMYOPATHY | STRESS | DNA MUTATIONS | 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
Myocardial infarction (MI) results in loss of cardiomyocytes, adverse extracellular matrix (ECM) and structural remodeling, and left ventricular (LV) dilation... 
Remodeling | Tissue inhibitor of metalloproteinases 3 | remodeling | ACTIVATION | CARDIAC & CARDIOVASCULAR SYSTEMS | PHYSIOLOGY | tissue inhibitor of metalloproteinases 3 | POSTMYOCARDIAL INFARCTION | HEART-FAILURE | DIASTOLIC DYSFUNCTION | MATRIX METALLOPROTEINASES | DISINTEGRIN | TISSUE INHIBITOR | PERIPHERAL VASCULAR DISEASE | BIOMECHANICAL STRESS | MICE | WALL-MOTION SCORE | 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 | Angiogenesis | Protein expression | Heart attacks | Matrix | Effects | Rodents | Index Medicus
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6. Full Text PTEN-inducible kinase 1 (PINK1)/Park6 is indispensable for normal heart function
by Filio Billia and Ludger Hauck and Filip Konecny and Vivek Rao and Jie Shen and Tak Wah Mak
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 6/2011, Volume 108, Issue 23, pp. 9572 - 9577
Oxidative stress is caused by an imbalance between reactive oxygen species (ROS) production and the ability of an organism to eliminate these toxic... 
Heart | Oxidative stress | Cardiomegaly | Mitochondria | Messenger RNA | Myocardium | Parkinson disease | Mice | Hypertrophy | Apoptosis | Mitochonopathy | Mitochondrial swelling | Mitochondrial energetics | OXIDATIVE STRESS | ACONITASE | MULTIDISCIPLINARY SCIENCES | MITOCHONDRIA | FAILURE | HYPERTROPHY | PINK1 | GROWTH | GENE-EXPRESSION | mitochonopathy | MICE | mitochondrial energetics | mitochondrial swelling | PARKINSONS-DISEASE | Protein Kinases - metabolism | Protein Kinases - genetics | Rats, Wistar | Heart Failure - enzymology | Humans | Middle Aged | Cardiomegaly - pathology | Male | Time Factors | Ventricular Dysfunction, Left - genetics | Myocardium - metabolism | Membrane Potential, Mitochondrial | Ventricular Dysfunction, Left - pathology | Ventricular Dysfunction, Left - enzymology | Adult | Female | Animals, Newborn | Cells, Cultured | Rats | Heart Failure - genetics | Cardiomegaly - enzymology | Heart Failure - pathology | Reverse Transcriptase Polymerase Chain Reaction | Blotting, Western | Mice, Knockout | Myocardium - enzymology | Animals | Myocytes, Cardiac - metabolism | Mutation | Cardiomegaly - genetics | Microscopy, Fluorescence | Heart failure | Oxygen | Rodents | Parkinsons disease | Homeostasis | Index Medicus | Biological Sciences
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7. 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
Age-related diastolic dysfunction has been attributed to an increased passive stiffness, which is regulated by extracellular matrix (ECM). We recently showed... 
Diastolic function | Extracellular matrix | Matrix metalloproteinase | Ageing | Collagen | CARDIAC & CARDIOVASCULAR SYSTEMS | TGF-BETA | ANGIOGENESIS | PROTECTION | HEART-FAILURE | FIBROBLASTS | MATRIX METALLOPROTEINASES | CARDIAC-HYPERTROPHY | PERIOSTIN EXPRESSION | REVEALS | 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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8. Full Text Critical Role of the NAD(P)H Oxidase Subunit p47phox for Left Ventricular Remodeling/Dysfunction and Survival After Myocardial Infarction
by Doerries, Carola and Grote, Karsten and Hilfiker-Kleiner, Denise and Luchtefeld, Maren and Schaefer, Arnd and Holland, Steven M and Sorrentino, Sajoscha and Manes, Costantina and Schieffer, Bernhard and Drexler, Helmut and Landmesser, Ulf
Circulation Research, ISSN 0009-7330, 03/2007, Volume 100, Issue 6, pp. 894 - 903
Accumulating evidence suggests a critical role of increased reactive oxygen species production for left ventricular (LV) remodeling and dysfunction after... 
Heart failure | Myocardial infarction | Superoxide anion | Remodeling | NAD(P)H oxidase | NADPH Oxidases - metabolism | Apoptosis - genetics | Ventricular Dysfunction, Left - genetics | Myocardial Infarction - pathology | Myocardium - metabolism | Superoxides - metabolism | NADPH Oxidases - genetics | Ventricular Dysfunction, Left - enzymology | Ventricular Remodeling - genetics | Myocardial Infarction - physiopathology | Heart Function Tests | Xanthine Oxidase - antagonists & inhibitors | Disease Models, Animal | Myocardial Infarction - enzymology | Xanthine Oxidase - metabolism | Electron Spin Resonance Spectroscopy | Matrix Metalloproteinase 2 - metabolism | Enzyme Inhibitors - pharmacology | Survival Rate | Disease Progression | Mice, Knockout | Myocardium - enzymology | Animals | Mice | Enzyme Activation - genetics | Nitric Oxide - metabolism | Ventricular Remodeling - drug effects | Index Medicus
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9. Full Text Phosphoinositide 3-kinase (p110α) gene delivery limits diabetes-induced cardiac NADPH oxidase and cardiomyopathy in a mouse model with established diastolic dysfunction
by Prakoso, Darnel and De Blasio, Miles J and Qin, Chengxue and Rosli, Sarah and Kiriazis, Helen and Qian, Hongwei and Du, Xiao-Jun and Weeks, Kate L and Gregorevic, Paul and McMullen, Julie R and Ritchie, Rebecca H
Clinical Science, ISSN 0143-5221, 06/2017, Volume 131, Issue 12, pp. 1345 - 1360
Phosphoinositide 3-kinase [PI3K (p110 alpha)] is able to negatively regulate the diabetes-induced increase in NADPH oxidase in the heart. Patients affected by... 
FIBROSIS | MEDICINE, RESEARCH & EXPERIMENTAL | HYPERTROPHY | APOPTOSIS | OXIDATIVE STRESS | SIGNALING PATHWAYS | HYPERGLYCEMIA | HEART-FAILURE | THERAPEUTIC STRATEGIES | MICE | MECHANISMS | Dependovirus - genetics | Diastole | Ventricular Function, Left | NADPH Oxidases - metabolism | Male | Diabetic Cardiomyopathies - physiopathology | Ventricular Remodeling | Time Factors | Ventricular Dysfunction, Left - genetics | Ventricular Dysfunction, Left - enzymology | Diabetic Cardiomyopathies - prevention & control | Diabetes Mellitus, Experimental - complications | Diabetic Cardiomyopathies - enzymology | Phosphatidylinositol 3-Kinase - biosynthesis | Transduction, Genetic | Signal Transduction | Myocardium - pathology | Ventricular Dysfunction, Left - physiopathology | Ventricular Dysfunction, Left - prevention & control | Diabetic Cardiomyopathies - genetics | Myocardium - enzymology | Animals | Phosphatidylinositol 3-Kinase - genetics | Mice | Genetic Vectors | Genetic Therapy - methods | Index Medicus
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10. 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
TNF-alpha (TNF-alpha) causes left ventricular diastolic dysfunction. Down-regulation of sarcoplasmic reticulum Ca2+-ATPase 2a protein (SERCA2a) expression is... 
Diastolic dysfunction | SERCA2a | TNF-α | Transcription | Simvastatin | Atp2a2 | APOPTOSIS | CARDIAC & CARDIOVASCULAR SYSTEMS | TNF-alpha | HEART-FAILURE | PRESERVED EJECTION FRACTION | CARDIOMYOCYTES | TUMOR-NECROSIS-FACTOR | INHIBITION | INFLAMMATION | atp2a2 | CARDIAC CONTRACTILITY | ROSUVASTATIN | MODULATION | 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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11. Full Text Metformin prevents progression of heart failure in dogs role of AMP-activated protein kinase
by Sasaki, Hideyuki and Asanuma, Hiroshi and Fujita, Masashi and Takahama, Hiroyuki and Wakeno, Masakatsu and Ito, Shin and Ogai, Akiko and Asakura, Masanori and Kim, Jiyoong and Minamino, Tetsuo and Takashima, Seiji and Sanada, Shoji and Sugimachi, Masaru and Komamura, Kazuo and Mochizuki, Naoki and Kitakaze, Masafumi
Circulation, ISSN 0009-7322, 05/2009, Volume 119, Issue 19, pp. 2568 - 2577
Background-Some studies have shown that metformin activates AMP-activated protein kinase (AMPK) and has a potent cardioprotective effect against... 
Heart failure | Metformin | AMP-activated protein kinase | Nitric oxide | heart failure | nitric oxide | CARDIAC & CARDIOVASCULAR SYSTEMS | ENDOTHELIAL NO SYNTHASE | BLOOD-GLUCOSE | metformin | ENDOPLASMIC-RETICULUM STRESS | DILATED CARDIOMYOPATHY | CONSCIOUS DOGS | NITRIC-OXIDE PRODUCTION | MYOCARDIAL FATTY-ACID | IN-VIVO | PERIPHERAL VASCULAR DISEASE | INDUCED CARDIAC-HYPERTROPHY | GLUCOSE-UPTAKE | HEMATOLOGY | Metformin - therapeutic use | Rats, Wistar | Apoptosis - drug effects | Heart Failure - enzymology | Nitric Oxide Synthase Type III - biosynthesis | Natriuretic Peptides - biosynthesis | Aminoimidazole Carboxamide - pharmacology | Cardiotonic Agents - therapeutic use | Myocytes, Cardiac - enzymology | Ribonucleotides - pharmacology | Protein Processing, Post-Translational - drug effects | Ventricular Dysfunction, Left - genetics | Ultrasonography | Ventricular Dysfunction, Left - enzymology | Heart Failure - diagnostic imaging | Phosphorylation - drug effects | Drug Evaluation, Preclinical | Transforming Growth Factor beta1 - biosynthesis | Natriuretic Peptides - genetics | Pyrazoles - pharmacology | Nitric Oxide - biosynthesis | Cells, Cultured - drug effects | AMP-Activated Protein Kinases - antagonists & inhibitors | Insulin Resistance | Rats | Transforming Growth Factor beta1 - genetics | Pyrimidines - pharmacology | Nitric Oxide Synthase Type III - genetics | Cells, Cultured - enzymology | Disease Progression | Ventricular Dysfunction, Left - diagnostic imaging | Heart Failure - drug therapy | Gene Expression Regulation - drug effects | AMP-Activated Protein Kinases - physiology | Animals | Myocytes, Cardiac - drug effects | Ventricular Dysfunction, Left - drug therapy | Aminoimidazole Carboxamide - analogs & derivatives | Dogs | Fibrosis | Oxidative Stress - drug effects | Prevention | Oxidative stress | Usage | Demographic aspects | Animal models in research | Physiological aspects | Dosage and administration | Cyclic adenylic acid | Research | Protein kinases | Index Medicus | Abridged Index Medicus
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12. Full Text Early matrix metalloproteinase-12 inhibition worsens post-myocardial infarction cardiac dysfunction by delaying inflammation resolution
by Iyer, Rugmani Padmanabhan and Patterson, Nicolle L and Zouein, Fouad A and Ma, Yonggang and Dive, Vincent and de Castro Brás, Lisandra E and Lindsey, Merry L
International Journal of Cardiology, ISSN 0167-5273, 2015, Volume 185, pp. 198 - 208
Abstract Rationale Matrix metalloproteinases (MMPs) regulate remodeling of the left ventricle (LV) post-myocardial infarction (MI). MMP-12 has potent... 
Cardiovascular | MMP-12 | LV remodeling | Neutrophil | CD44 | Proteomics | Apoptosis | CARDIAC & CARDIOVASCULAR SYSTEMS | HUMAN NEUTROPHILS | MYOCARDIAL-INFARCTION | MOUSE | RECEPTOR | MODEL | MACROPHAGE ELASTASE MMP-12 | METALLOELASTASE | EXPRESSION | Immunohistochemistry | Immunoblotting | Male | Matrix Metalloproteinase 12 - genetics | RNA - genetics | Ventricular Dysfunction, Left - genetics | Ventricular Dysfunction, Left - enzymology | Ventricular Function, Left - physiology | Real-Time Polymerase Chain Reaction | Disease Models, Animal | Myocardial Infarction - enzymology | Mice, Inbred C57BL | Ventricular Function, Left - drug effects | Gene Expression Regulation | Ventricular Dysfunction, Left - etiology | Ventricular Remodeling - physiology | Matrix Metalloproteinase Inhibitors - pharmacology | Myocardial Infarction - complications | Animals | Myocardial Infarction - drug therapy | Inflammation - genetics | Matrix Metalloproteinase 12 - biosynthesis | Mice | Matrix Metalloproteinase 12 - drug effects | Inflammation - enzymology | Heart attack | Index Medicus | apoptosis | proteomics | neutrophil
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13. Full Text Deriving a cardiac ageing signature to reveal MMP-9-dependent inflammatory signalling in senescence
by Ma, Yonggang and Chiao, Ying Ann and Clark, Ryan and Flynn, Elizabeth R and Yabluchanskiy, Andriy and Ghasemi, Omid and Zouein, Fouad and Lindsey, Merry L and Jin, Yu-Fang
Cardiovascular Research, ISSN 0008-6363, 06/2015, Volume 106, Issue 3, pp. 421 - 431
Aims Cardiac ageing involves the progressive development of cardiac fibrosis and diastolic dysfunction coordinated by MMP-9. Here, we report a cardiac ageing... 
Inflammation | Cardiac ageing | Macrophage polarization | MMP-9 | Proteomics | ACTIVATION | CARDIAC & CARDIOVASCULAR SYSTEMS | MYOCARDIAL-INFARCTION | ANGIOGENESIS | TISSUE | DELETION | MATRIX-METALLOPROTEINASE-9 | MICE | ACCUMULATION | AGE | Hypertrophy, Left Ventricular - enzymology | Age Factors | Diastole | Ventricular Function, Left | Myocytes, Cardiac - immunology | Male | Gene Expression Profiling | Myocytes, Cardiac - enzymology | Matrix Metalloproteinase 9 - metabolism | Ventricular Remodeling | Hypertrophy, Left Ventricular - genetics | Aging - genetics | Cellular Senescence | Hypertrophy, Left Ventricular - pathology | Matrix Metalloproteinase 9 - genetics | Inflammation Mediators - metabolism | Ventricular Dysfunction, Left - pathology | Ventricular Dysfunction, Left - enzymology | Female | Macrophages - immunology | Signal Transduction | Hypertrophy, Left Ventricular - prevention & control | Mice, Inbred C57BL | Cell Communication | Matrix Metalloproteinase 9 - deficiency | Ventricular Dysfunction, Left - physiopathology | Aging - pathology | Macrophages - enzymology | Mice, Knockout | Myocytes, Cardiac - pathology | Hypertrophy, Left Ventricular - immunology | Phenotype | Animals | Fibrosis | Hypertrophy, Left Ventricular - physiopathology | Aging - metabolism | Index Medicus | Original
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