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JACC (Journal of the American College of Cardiology), ISSN 0735-1097, 2014, Volume 64, Issue 24, pp. 2589 - 2600
Abstract Background Mild hypertrophy but increased arrhythmic risk characterizes the stereotypic phenotype proposed for hypertrophic cardiomyopathy (HCM)... 
Cardiovascular | Internal Medicine | end-stage | diastolic function | troponin | triphasic filling | genotype to phenotype correlation | correlation triphasic filling troponin | genotype to phenotype | diastolic function end-stage | CARDIAC & CARDIOVASCULAR SYSTEMS | CARDIOVASCULAR MAGNETIC-RESONANCE | HEARTS BEARING | PREVALENCE | LEFT-VENTRICULAR HYPERTROPHY | TASK-FORCE | CARDIAC TROPONIN-T | DISEASE | DYSFUNCTION | ALPHA-TROPOMYOSIN | DOPPLER-ECHOCARDIOGRAPHY | Follow-Up Studies | Humans | Middle Aged | Male | Cardiomyopathy, Hypertrophic - complications | Death, Sudden, Cardiac - etiology | Ventricular Fibrillation - etiology | Ventricular Outflow Obstruction - etiology | Actins - genetics | Ventricular Dysfunction, Left - genetics | Ventricular Fibrillation - genetics | Adult | Female | Heart Function Tests | Actin Cytoskeleton - genetics | Severity of Illness Index | Troponin T - genetics | Ventricular Outflow Obstruction - genetics | Cardiomyopathy, Hypertrophic - genetics | Genetic Predisposition to Disease | MAP Kinase Kinase Kinases - genetics | Ventricular Dysfunction, Left - etiology | Patient Outcome Assessment | Cardiomyopathy, Hypertrophic - diagnosis | Disease Progression | Cardiomyopathy, Hypertrophic - physiopathology | Italy | Mutation | Sects | Genetic aspects | Cardiomyopathy, Hypertrophic | Gene mutations | Heart | Medical research | Tachycardia | Actin | Genes | Myosin | Medicine, Experimental | Protein binding | Heart attacks | Cardiology | Drug therapy | Clinical outcomes | MYH7, myosin heavy chain | TNNT2, cardiac troponin T gene | HR, hazard ratio | SCD, sudden cardiac death | ICD, implantable cardioverter-defibrillator | TPM1, cardiac α-tropomyosin gene | LVH, left ventricular hypertrophy | MYBPC3, myosin binding protein C | LV, left ventricular | ECG, electrocardiography | LGE, late gadolinium enhancement | AF, atrial fibrillation | NSVT, nonsustained ventricular tachycardia | ACTC, cardiac α-actin gene | Original Investigation | CMR, cardiac magnetic resonance | HCM, hypertrophic cardiomyopathy | TNNI3, cardiac troponin I gene | NYHA, New York Heart Association
Journal Article
Arteriosclerosis, Thrombosis, and Vascular Biology, ISSN 1079-5642, 04/2016, Volume 36, Issue 4, pp. 636 - 646
OBJECTIVE—Basigin (Bsg) is a transmembrane glycoprotein that activates matrix metalloproteinases and promotes inflammation. However, the role of Bsg in the... 
heart failure | cytokines | hypertrophy | inflammation | angiotensin II | INHIBITS EMMPRIN | CHRONIC HEART-FAILURE | RECEPTOR | CANCER | METALLOPROTEINASE INDUCER EMMPRIN | PMA-INDUCED MACROPHAGES | ACTIVATES PLATELETS | PERIPHERAL VASCULAR DISEASE | CD147 | HEMATOLOGY | EXPRESSION | Oxidative Stress | Heart Failure - physiopathology | Male | Aortic Diseases - metabolism | Heart Failure - prevention & control | Hypertrophy, Left Ventricular - genetics | Time Factors | Ventricular Dysfunction, Left - genetics | Basigin - genetics | Myocardium - metabolism | Proto-Oncogene Proteins c-akt - metabolism | Heart Failure - etiology | Disease Models, Animal | Fibroblasts - metabolism | Animals, Newborn | Angiotensin II - pharmacology | Hypertrophy, Left Ventricular - prevention & control | Rats | Heart Failure - genetics | Heart Failure - metabolism | Fibroblasts - pathology | Mice, Knockout | Ventricular Dysfunction, Left - metabolism | Myocytes, Cardiac - pathology | Aortic Diseases - genetics | Myocytes, Cardiac - drug effects | Fibroblasts - drug effects | Fibrosis | Myocytes, Cardiac - metabolism | Hypertrophy, Left Ventricular - physiopathology | Rats, Wistar | Ventricular Function, Left | JNK Mitogen-Activated Protein Kinases - metabolism | Extracellular Signal-Regulated MAP Kinases - metabolism | Blood Proteins - metabolism | Hypertrophy, Left Ventricular - pathology | Inflammation Mediators - metabolism | Ventricular Dysfunction, Left - pathology | Hypertrophy, Left Ventricular - etiology | Hypertrophy, Left Ventricular - metabolism | Cells, Cultured | Ventricular Dysfunction, Left - etiology | Myocardium - pathology | Heart Failure - pathology | Ventricular Dysfunction, Left - physiopathology | Ventricular Dysfunction, Left - prevention & control | Mechanotransduction, Cellular | Aortic Diseases - physiopathology | Animals | Aortic Diseases - complications | Basigin - metabolism | Matrix Metalloproteinases - metabolism
Journal Article
The International Journal of Cardiovascular Imaging, ISSN 1569-5794, 4/2015, Volume 31, Issue 4, pp. 669 - 679
Consistent protocols for the assessment of diastolic and systolic cardiac function to assure the comparability of existing data on preclinical models are... 
Heart failure | Echocardiography | Medicine & Public Health | Magnetic resonance imaging | Cardiac disease | Electrocardiography | Cardiology | Doppler | INBRED MOUSE STRAINS | CARDIAC & CARDIOVASCULAR SYSTEMS | MRI | HEART-FAILURE | MODEL | ECHOCARDIOGRAPHIC-ASSESSMENT | CARDIAC-HYPERTROPHY | IN-VIVO | RADIOLOGY, NUCLEAR MEDICINE & MEDICAL IMAGING | Predictive Value of Tests | Hypertrophy, Left Ventricular - enzymology | Ventricular Function, Left | Ventricular Dysfunction, Right - genetics | Heart Failure - enzymology | Heart Failure - physiopathology | Hypertrophy, Left Ventricular - diagnosis | Myosin Heavy Chains - genetics | Male | Cardiomyopathy, Hypertrophic - enzymology | Ventricular Dysfunction, Right - enzymology | Hypertrophy, Right Ventricular - physiopathology | Ventricular Remodeling | Calcineurin - genetics | Hypertrophy, Left Ventricular - genetics | Ventricular Dysfunction, Left - genetics | Echocardiography, Doppler | Ventricular Dysfunction, Left - enzymology | Female | Ventricular Dysfunction, Right - physiopathology | Heart Failure - diagnosis | Hypertrophy, Right Ventricular - genetics | Disease Models, Animal | High-Throughput Screening Assays - methods | Promoter Regions, Genetic | Cardiomyopathy, Hypertrophic - genetics | Genetic Predisposition to Disease | Hypertrophy, Right Ventricular - diagnosis | Mice, Inbred C57BL | Heart Failure - genetics | Mice, Transgenic | Ventricular Dysfunction, Left - diagnosis | Hypertrophy, Right Ventricular - enzymology | Ventricular Dysfunction, Right - diagnosis | Cardiomyopathy, Hypertrophic - diagnosis | Disease Progression | Ventricular Dysfunction, Left - physiopathology | Magnetic Resonance Imaging | Phenotype | Animals | Cardiomyopathy, Hypertrophic - physiopathology | Hemodynamics | Hypertrophy, Left Ventricular - physiopathology | Calcineurin - metabolism | Ventricular Function, Right | Ventricular Myosins - genetics | Heart | Genetic engineering | Electrocardiogram
Journal Article
Arteriosclerosis, Thrombosis, and Vascular Biology, ISSN 1079-5642, 07/2014, Volume 34, Issue 7, pp. 1399 - 1411
OBJECTIVE—S100A12 and fibroblast growth factor 23 are biomarkers of cardiovascular morbidity and mortality in patients with chronic kidney disease (CKD). We... 
renal insufficiency chronic | S100 proteins | glycosylation end products advanced | hypertrophy left ventricular | MORTALITY | PLASMA S100A12 LEVELS | renal insufficiency, chronic | VASCULAR CALCIFICATION | hypertrophy, left ventricular | ATHEROSCLEROSIS | RAGE | ARTERIAL CALCIFICATION | glycosylation end products, advanced | GROWTH-FACTOR 23 | HEMODIALYSIS-PATIENTS | PERIPHERAL VASCULAR DISEASE | HEMATOLOGY | EXPRESSION | SOLUBLE RECEPTOR | Calgranulin B - metabolism | Diastole | Humans | Calgranulin A - genetics | Renal Insufficiency, Chronic - complications | Sclerosis | S100A12 Protein | Fibroblast Growth Factors - metabolism | Inflammation - metabolism | S100 Proteins - genetics | Hypertrophy, Left Ventricular - genetics | Calcinosis - etiology | Time Factors | Myocardium - metabolism | Renal Insufficiency, Chronic - genetics | Receptor for Advanced Glycation End Products | Disease Models, Animal | Fibroblasts - metabolism | Signal Transduction | Receptors, Immunologic - deficiency | Genotype | Mice, Transgenic | S100 Proteins - metabolism | Mice, Knockout | Ventricular Dysfunction, Left - metabolism | Phenotype | Heart Valve Diseases - metabolism | Heart Valve Diseases - genetics | Mice | Hypertrophy, Left Ventricular - physiopathology | Receptors, Immunologic - genetics | Heart Valve Diseases - pathology | Ventricular Function, Left | Calgranulin A - metabolism | Leukocyte L1 Antigen Complex - metabolism | Aortic Valve - pathology | Renal Insufficiency, Chronic - metabolism | Inflammation - complications | Ventricular Remodeling | Inflammation Mediators - metabolism | Calgranulin B - genetics | Calcinosis - metabolism | Hypertrophy, Left Ventricular - etiology | Hypertrophy, Left Ventricular - metabolism | Mice, Inbred C57BL | Cells, Cultured | Ventricular Dysfunction, Left - etiology | Heart Valve Diseases - etiology | Aortic Valve - metabolism | Ventricular Dysfunction, Left - physiopathology | Animals | Inflammation - genetics | Leukocyte L1 Antigen Complex - genetics | Receptors, Immunologic - metabolism
Journal Article
European Heart Journal, ISSN 0195-668X, 2017, Volume 38, Issue 46, pp. 3449 - 3460
Journal Article
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
Journal Article
American Journal of Physiology - Heart and Circulatory Physiology, ISSN 0363-6135, 08/2013, Volume 305, Issue 3, pp. H397 - H402
The C57BL/6 mouse strain is one of the most commonly used in experimental research. It is known to differ from other strains in baseline cardiovascular... 
C57BL/6 mouse | Heart failure | Cardiac hypertrophy | Substrain | TAC | heart failure | HYPERTROPHY | CARDIAC & CARDIOVASCULAR SYSTEMS | PHYSIOLOGY | GENE | PERIPHERAL VASCULAR DISEASE | substrain | cardiac hypertrophy | BLOOD-PRESSURE | MOUSE MODELS | Adaptation, Physiological | Species Specificity | Ventricular Function, Left | Heart Failure - physiopathology | Myosin Heavy Chains - genetics | Male | RNA, Messenger - metabolism | Hypertrophy, Left Ventricular - genetics | Ligation | Time Factors | Ventricular Dysfunction, Left - genetics | Myocardium - metabolism | Ultrasonography | Aorta - physiopathology | Heart Failure - diagnostic imaging | Heart Failure - etiology | Disease Models, Animal | Biomarkers - metabolism | Myocardial Contraction | Natriuretic Peptide, Brain - genetics | Cardiac Myosins - genetics | Hypertrophy, Left Ventricular - etiology | Hypertrophy, Left Ventricular - metabolism | Mice, Inbred C57BL | Gene Expression Regulation | Ventricular Dysfunction, Left - etiology | Genotype | Heart Failure - genetics | Myocardium - pathology | Heart Failure - metabolism | Ventricular Dysfunction, Left - diagnostic imaging | Ventricular Dysfunction, Left - physiopathology | Ventricular Dysfunction, Left - metabolism | Phenotype | Animals | Aorta - surgery | Mice | Hypertrophy, Left Ventricular - physiopathology | Sarcoplasmic Reticulum Calcium-Transporting ATPases - genetics | Hypertrophy, Left Ventricular - diagnostic imaging | Heart enlargement | Physiological aspects | Blood pressure | Genetic aspects | Research | Gene expression | Health aspects | 6 mouse | C57BL | Integrative Cardiovascular Physiology and Pathophysiology
Journal Article
American Journal of Physiology - Heart and Circulatory Physiology, ISSN 0363-6135, 05/2019, Volume 316, Issue 5, pp. H1224 - H1228
A novel transgenic rat strain has recently been generated that stably expresses the genetically engineered calcium sensor protein GCaMP2 in different cell... 
Diastolic dysfunction | Calcium sensor transgenic rat | Calcium homeostasis | Left ventricular pressure-volume analysis | Left ventricular function | HOMEOSTASIS | CARDIAC & CARDIOVASCULAR SYSTEMS | PHYSIOLOGY | left ventricular function | left ventricular pressure-volume analysis | STIFFNESS | HEART-FAILURE | diastolic dysfunction | RELAXATION | PERIPHERAL VASCULAR DISEASE | calcium homeostasis | calcium sensor transgenic rat | Ventricular Function, Left | Male | Green Fluorescent Proteins - genetics | Hypertension - etiology | Ventricular Remodeling | Arterial Pressure | Hypertrophy, Left Ventricular - genetics | Ventricular Dysfunction, Left - genetics | Green Fluorescent Proteins - toxicity | Myocardium - metabolism | Hypertension - genetics | Green Fluorescent Proteins - metabolism | Vascular Resistance | Rats, Transgenic | Hypertrophy, Left Ventricular - etiology | Hypertrophy, Left Ventricular - metabolism | Ventricular Dysfunction, Left - etiology | Genotype | Rats, Sprague-Dawley | Hypertension - physiopathology | Ventricular Dysfunction, Left - physiopathology | Hypertension - metabolism | Stroke Volume | Ventricular Dysfunction, Left - metabolism | Phenotype | Animals | Biosensing Techniques | Ventricular Pressure | Hemodynamics | Hypertrophy, Left Ventricular - physiopathology | Heart | Hypertension | Calcium | Homeostasis | Fluorescence | Cardiomyocytes | Parameter sensitivity | Contraction | Weight | Proteins | Autopsy | Rodents | Genetic engineering | In vivo methods and tests | Blood pressure | Sensors | Ventricle | Hypertrophy
Journal Article
Journal of Applied Physiology, ISSN 8750-7587, 01/2013, Volume 114, Issue 1, pp. 131 - 147
We have previously reported chronic low-intensity interval exercise training attenuates fibrosis, impaired cardiac mitochondrial function, and coronary... 
Diastolic heart failure | Exercise | Coronary flow | Fibrosis | MVO | Speckle tracking | Hypertrophic signaling | Protein Kinases - genetics | Connectin | Heart - physiology | Natriuretic Peptide, Brain - metabolism | Ventricular Function, Left - genetics | Heart Failure - physiopathology | Extracellular Matrix - metabolism | Male | Oxygen Consumption - physiology | Tissue Inhibitor of Metalloproteinases - genetics | Hypertrophy, Left Ventricular - genetics | Swine | Myocardium - metabolism | Ventricular Remodeling - genetics | Sarcomeres - physiology | Proto-Oncogene Proteins c-akt - metabolism | Natriuretic Peptide, Brain - genetics | Fibrosis - physiopathology | Matrix Metalloproteinase 2 - metabolism | Sarcomeres - metabolism | Diastole - genetics | Heart Failure - genetics | Heart Failure - metabolism | Arterial Pressure - physiology | Diastole - physiology | Muscle Proteins - genetics | Matrix Metalloproteinase 2 - genetics | MAP Kinase Kinase 4 - genetics | Hypertrophy, Left Ventricular - physiopathology | Regional Blood Flow - physiology | Protein Kinases - metabolism | Regional Blood Flow - genetics | Myocardial Contraction - physiology | Collagen Type III - metabolism | Fibrosis - metabolism | Oxygen - metabolism | Proto-Oncogene Proteins c-akt - genetics | Extracellular Matrix - genetics | Myocardial Contraction - genetics | Arterial Pressure - genetics | MAP Kinase Kinase 4 - metabolism | Sarcomeres - genetics | Muscle Proteins - metabolism | Ventricular Function, Left - physiology | Citrate (si)-Synthase - metabolism | Heart Failure - rehabilitation | Fibrosis - genetics | Hypertrophy, Left Ventricular - metabolism | RNA, Messenger - genetics | Collagen Type III - genetics | Ventricular Remodeling - physiology | Physical Conditioning, Animal - physiology | Tissue Inhibitor of Metalloproteinases - metabolism | Animals | Oxygen Consumption - genetics | Citrate (si)-Synthase - genetics | speckle tracking | coronary flow | hypertrophic signaling | exercise | fibrosis | diastolic heart failure | MV̇o2
Journal Article
Journal of the American Heart Association, ISSN 2047-9980, 01/2016, Volume 5, Issue 1, p. n/a
Background Mitochondrial reactive oxygen species (ROS) are associated with metabolic heart disease (MHD). However, the mechanism by which ROS cause MHD is... 
metabolic heart disease | mitochondria | obesity | oxidative protein modifications | oxidative stress | Obesity | Oxidative stress | Metabolic heart disease | Mitochondria | Oxidative protein modifications | EXTREME OBESITY | CARDIAC & CARDIOVASCULAR SYSTEMS | UNCOUPLING PROTEINS | MECHANISMS | DIABETIC CARDIOMYOPATHY | SUCCINATE-DEHYDROGENASE | COMPLEX-II | PROTEIN S-GLUTATHIONYLATION | MICE | DYSFUNCTION | Mitochondrial Diseases - pathology | Mitochondria, Heart - metabolism | Reactive Oxygen Species - metabolism | Oxidative Stress | Ventricular Function, Left | Mitochondria, Heart - pathology | Mitochondrial Diseases - metabolism | Electron Transport Complex I - metabolism | Mitochondrial Diseases - etiology | Hypertrophy, Left Ventricular - genetics | Ventricular Dysfunction, Left - genetics | Hypertrophy, Left Ventricular - pathology | Adenosine Triphosphate - metabolism | Diet, High-Fat | Ventricular Dysfunction, Left - pathology | Dietary Sucrose | Disease Models, Animal | Mitochondrial Diseases - genetics | Mitochondrial Diseases - prevention & control | Electron Transport Complex II - genetics | Oxidation-Reduction | Catalase - genetics | Hypertrophy, Left Ventricular - etiology | Hypertrophy, Left Ventricular - metabolism | Hypertrophy, Left Ventricular - prevention & control | Mice, Inbred C57BL | Ventricular Dysfunction, Left - etiology | Mice, Transgenic | Ventricular Dysfunction, Left - physiopathology | Ventricular Dysfunction, Left - prevention & control | Catalase - metabolism | Ventricular Dysfunction, Left - metabolism | Animals | Energy Metabolism | Electron Transport Complex II - metabolism | Protein Processing, Post-Translational | Hypertrophy, Left Ventricular - physiopathology | Mutation | Mitochondrial Diseases - physiopathology
Journal Article
American Journal of Physiology - Heart and Circulatory Physiology, ISSN 0363-6135, 2015, Volume 309, Issue 11, pp. H1827 - H1836
The mammalian circadian clock consists of multiple transcriptional regulators that coordinate biological processes in a time-of-day-dependent manner.... 
Circadian clock | Aging | Diastolic dysfunction | Extracellular matrix | Inflammation | Bmal1 | RESPONSIVENESS | CARDIAC & CARDIOVASCULAR SYSTEMS | PHYSIOLOGY | MYOCARDIAL-INFARCTION | HEART-FAILURE | circadian clock | BLOOD-PRESSURE | HYPERTROPHY | inflammation | GENES | diastolic dysfunction | PERIPHERAL VASCULAR DISEASE | aging | RHYTHM | OSCILLATIONS | EXPRESSION | extracellular matrix | Age Factors | Diastole | Ventricular Function, Left | Extracellular Matrix - metabolism | Male | Smad3 Protein - metabolism | RNA, Messenger - metabolism | Extracellular Matrix - genetics | ARNTL Transcription Factors - deficiency | Inflammation - metabolism | Ventricular Remodeling | Hypertrophy, Left Ventricular - genetics | Time Factors | Ventricular Dysfunction, Left - genetics | Hypertrophy, Left Ventricular - pathology | Inflammation Mediators - metabolism | Ventricular Dysfunction, Left - pathology | Transcription, Genetic | ARNTL Transcription Factors - genetics | Signal Transduction | Hypertrophy, Left Ventricular - metabolism | Mice, Inbred C57BL | Gene Expression Regulation | Smad2 Protein - metabolism | Genotype | Disease Progression | Ventricular Dysfunction, Left - physiopathology | Mice, Knockout | Ventricular Dysfunction, Left - metabolism | Myocytes, Cardiac - pathology | Phenotype | Animals | Fibrosis | Inflammation - genetics | Myocytes, Cardiac - metabolism | Hypertrophy, Left Ventricular - physiopathology | Transforming Growth Factor beta - metabolism | Gene expression | Collagen | Circadian rhythms | Heart cells | Genetic aspects | Cardiovascular diseases | Health aspects | Call for Papers
Journal Article
Cardiovascular Research, ISSN 0008-6363, 2017, Volume 113, Issue 7, pp. 760 - 769
Aims Elabela/Toddler/Apela (ELA) has been identified as a novel endogenous peptide ligand for APJ/Apelin receptor/ Aplnr. ELA plays a crucial role in early... 
ACE2 | ACE | APJ | Elabela | Angiotensin | Apelin | CONVERTING ENZYME 2 | ENDOGENOUS LIGAND | CARDIAC & CARDIOVASCULAR SYSTEMS | HYPOTENSIVE ACTION | CONTRACTILITY | APELIN RECEPTOR | FAILING HEARTS | HYPERTROPHY | PATHWAY | IN-VIVO | Humans | Heart Failure - physiopathology | Apelin Receptors - deficiency | Myocardial Contraction - drug effects | Male | Heart Failure - prevention & control | Ventricular Dysfunction, Left - genetics | Myocardium - metabolism | Peptidyl-Dipeptidase A - metabolism | Hypertension - genetics | Heart Failure - etiology | Disease Models, Animal | Constriction | Hypertrophy, Left Ventricular - prevention & control | Ventricular Function, Left - drug effects | Heart Failure - genetics | Cardiotonic Agents - pharmacology | Hypertension - metabolism | Mice, Knockout | Ventricular Dysfunction, Left - metabolism | Cardiotonic Agents - administration & dosage | Signal Transduction - drug effects | Aorta - surgery | Fibrosis | Forkhead Box Protein M1 - genetics | Ligands | Hypertrophy, Left Ventricular - physiopathology | Peptide Hormones - pharmacology | Peptidyl-Dipeptidase A - genetics | Arterial Pressure | Transfection | Apelin Receptors - genetics | HEK293 Cells | Hypertension - prevention & control | Aorta - physiopathology | Angiotensin II | Peptide Hormones - administration & dosage | Hypertrophy, Left Ventricular - etiology | Hypertrophy, Left Ventricular - metabolism | Mice, Inbred C57BL | Gene Expression Regulation | Myocardium - pathology | Hypertension - physiopathology | Ventricular Dysfunction, Left - physiopathology | Ventricular Dysfunction, Left - prevention & control | Infusions, Subcutaneous | Apelin Receptors - metabolism | Animals | Forkhead Box Protein M1 - metabolism
Journal Article
American Journal of Physiology - Heart and Circulatory Physiology, ISSN 0363-6135, 09/2012, Volume 303, Issue 5, pp. H587 - H596
Garcia AG, Wilson RM, Heo J, Murthy NR, Baid S, Ouchi N, Sam F. Interferon-gamma ablation exacerbates myocardial hypertrophy in diastolic heart failure. Am J... 
Hypertension | Diastolic dysfunction | Aldosterone | Autophagy | CARDIAC-FUNCTION | CARDIAC & CARDIOVASCULAR SYSTEMS | PHYSIOLOGY | autophagy | RESISTANT HYPERTENSION | aldosterone | PRESERVED EJECTION FRACTION | PREVALENCE | LEFT-VENTRICULAR HYPERTROPHY | HEMODYNAMIC STRESS | diastolic dysfunction | PERIPHERAL VASCULAR DISEASE | MICE | DYSFUNCTION | hypertension | Heart Failure, Diastolic - genetics | Myocardium - immunology | Ventricular Function, Left | Myocytes, Cardiac - immunology | Male | Heart Failure, Diastolic - metabolism | Hypertension - etiology | Ventricular Remodeling | Hypertrophy, Left Ventricular - genetics | Nephrectomy | Time Factors | Ventricular Dysfunction, Left - genetics | Hypertrophy, Left Ventricular - pathology | Myocardium - metabolism | Inflammation Mediators - metabolism | Interferon-gamma - genetics | Interferon-gamma - deficiency | Disease Models, Animal | Hypertrophy, Left Ventricular - etiology | Hypertrophy, Left Ventricular - metabolism | Hypertrophy, Left Ventricular - prevention & control | Rats | Ventricular Dysfunction, Left - etiology | Myocardium - pathology | Heart Failure, Diastolic - pathology | Rats, Sprague-Dawley | Ventricular Dysfunction, Left - immunology | Disease Progression | Hypertension - physiopathology | Ventricular Dysfunction, Left - physiopathology | Hypertension - metabolism | Mice, Knockout | Stroke Volume | Heart Failure, Diastolic - physiopathology | Hypertrophy, Left Ventricular - immunology | Animals | Myocytes, Cardiac - drug effects | Heart Failure, Diastolic - etiology | Heart Failure, Diastolic - immunology | Interferon-gamma - administration & dosage | Fibrosis | Hypertension - complications | Myocytes, Cardiac - metabolism | Mice | Mice, Inbred BALB C | Hypertrophy, Left Ventricular - physiopathology | Integrative Cardiovascular Physiology and Pathophysiology
Journal Article