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Journal of Cardiovascular Translational Research, ISSN 1937-5387, 8/2016, Volume 9, Issue 4, pp. 374 - 399
In part 1, we considered cytomolecular mechanisms underlying calcific aortic valve disease (CAVD), hemodynamics, and adaptive feedbacks controlling... 
Replication of cardiomyocyte sarcomeres in-parallel and in-series | G protein-coupled receptors | Calcineurin | Fetal gene reexpression | Medicine/Public Health, general | Biomedicine general | Receptor tyrosine kinases | Biomedical Engineering | Aortic valvular stenosis | Mitochondrial biogenesis | Medicine & Public Health | Extracellular signal-regulated kinases 1 and 2 | Cardiology | Subendocardial ischemia | Mitogen-activated protein kinases | Human Genetics | Myocardial fibrosis | Physiological cardiac hypertrophy | Pressure overload | Transvalvular gradient | Resident endogenous stem/progenitor cells and myocardial regeneration | Pathological cardiac hypertrophy and failure | Blood flow | PI3K(p110α) lipid kinase–Akt serine/threonine kinase pathway | Concentric LV hypertrophy | Myocardial hypertrophic and hyperplastic growth | Cardiomyocyte apoptosis | MEDICINE, RESEARCH & EXPERIMENTAL | CARDIAC & CARDIOVASCULAR SYSTEMS | DIASTOLIC VORTEX FORCES | LONG NONCODING RNA | HEART-FAILURE | PI3K(p110 alpha)lipid kinase-Akt serine/threonine kinase pathway | CARDIAC STEM-CELLS | SYSTOLIC FUNCTION | MYOSIN HEAVY-CHAIN | RENIN-ANGIOTENSIN SYSTEM | CYCLASE TYPE 5 | MYOCARDIAL HYPERTROPHY | PRESSURE-OVERLOAD HYPERTROPHY | Calcinosis - genetics | Aortic Valve Stenosis - genetics | Calcinosis - complications | Cell Proliferation | Mitochondria, Heart - metabolism | Prognosis | Ventricular Function, Left | Mitochondria, Heart - pathology | Humans | Hyperplasia | Extracellular Matrix - metabolism | Male | Stem Cells - metabolism | Aortic Valve - pathology | Ventricular Remodeling | Hypertrophy, Left Ventricular - genetics | Female | Calcinosis - metabolism | Genetic Predisposition to Disease | Signal Transduction | Hypertrophy, Left Ventricular - etiology | Hypertrophy, Left Ventricular - metabolism | Risk Factors | Aortic Valve Stenosis - physiopathology | Gene Expression Regulation | Aortic Valve - physiopathology | Aortic Valve - metabolism | Aortic Valve Stenosis - complications | Animals | Sex Factors | Stem Cells - pathology | Aortic Valve Stenosis - metabolism | Hypertrophy, Left Ventricular - physiopathology | Extracellular Matrix - pathology | Apoptosis | Calcinosis - physiopathology | Heart | Tyrosine | Heart enlargement | Genes | Biosynthesis | Stress (Physiology) | DNA binding proteins | Genetic transcription | Heart valve diseases | Cellular signal transduction | G proteins | Mitogens | Protein kinases | threonine kinase pathway | PI3K(p110α) lipid kinase–Akt serine | Resident endogenous stem | progenitor cells and myocardial regeneration
Journal Article
Circulation Research, ISSN 0009-7330, 01/2009, Volume 104, Issue 2, pp. 265 - 275
Left ventricular (LV) hypertrophy commonly develops in response to chronic hypertension and is a significant risk factor for heart failure and death. The... 
Ubiquitin | Myocyte hypertrophy | Calcineurin | Estrogen | Pressure overload | Left ventricular remodeling | Proteasome | VITRO | proteasome | estrogen | PRESSURE-OVERLOAD | CARDIAC & CARDIOVASCULAR SYSTEMS | PROTEIN | MYOCARDIAL-INFARCTION | myocyte hypertrophy | TRANSCRIPTION | MCIP1 | calcineurin | pressure overload | ubiquitin | INHIBITION | CARDIAC-HYPERTROPHY | IN-VIVO | PERIPHERAL VASCULAR DISEASE | left ventricular remodeling | HEMATOLOGY | STRIATED-MUSCLES | Estradiol - analogs & derivatives | Receptors, Estrogen - metabolism | Hypertrophy, Left Ventricular - enzymology | Ventricular Function, Left | Ubiquitin - metabolism | Drug Implants | Estrogen Antagonists - pharmacology | Male | Myocytes, Cardiac - enzymology | Ventricular Remodeling | Calcineurin - genetics | Phenylephrine - pharmacology | Time Factors | Hypertrophy, Left Ventricular - pathology | Female | Estradiol - pharmacology | Disease Models, Animal | Animals, Newborn | Myocardial Contraction | Estradiol - metabolism | Ovariectomy | Hypertrophy, Left Ventricular - prevention & control | Mice, Inbred C57BL | NFATC Transcription Factors - metabolism | Cells, Cultured | Estradiol - administration & dosage | Receptors, Estrogen - antagonists & inhibitors | Cell Size | Mice, Transgenic | Myocardium - pathology | Mice, Knockout | Myocytes, Cardiac - pathology | Myocardium - enzymology | Animals | Myocytes, Cardiac - drug effects | Calcineurin - deficiency | Signal Transduction - drug effects | Mice | Hemodynamics | Hypertrophy, Left Ventricular - physiopathology | Proteasome Endopeptidase Complex - metabolism | Calcineurin - metabolism | NFATC Transcription Factors - genetics | Pressure Overload | Myocyte Hypertrophy | LV Remodeling
Journal Article
JACC: Cardiovascular Imaging, ISSN 1936-878X, 2016, Volume 10, Issue 11, pp. 1320 - 1333
Abstract Objectives Cardiac magnetic resonance (CMR) was used to investigate the extracellular compartment and myocardial fibrosis in patients with aortic... 
Cardiovascular | magnetic resonance imaging | fibrosis | myocardium | aortic stenosis | hypertrophy | T1 mapping | CARDIAC & CARDIOVASCULAR SYSTEMS | CORONARY | CARDIOVASCULAR MAGNETIC-RESONANCE | T1 VALUES | VALIDATION | ADENOSINE STRESS | DISEASE | VALVE-REPLACEMENT | OPTIMIZATION | PROGNOSTIC-SIGNIFICANCE | RADIOLOGY, NUCLEAR MEDICINE & MEDICAL IMAGING | Cardiomyopathies - diagnostic imaging | Prospective Studies | Ventricular Function, Left | Humans | Middle Aged | Heart Failure - physiopathology | Male | Cardiomyopathies - etiology | Case-Control Studies | Aortic Valve Stenosis - diagnostic imaging | Aortic Valve Stenosis - mortality | Cardiomyopathies - physiopathology | Ventricular Remodeling | Time Factors | Cardiomyopathies - mortality | Female | Heart Failure - diagnostic imaging | Heart Failure - etiology | Heart Failure - mortality | Hypertrophy, Left Ventricular - mortality | Echocardiography | Hypertrophy, Left Ventricular - etiology | Risk Factors | Aortic Valve Stenosis - physiopathology | Kaplan-Meier Estimate | Myocardium - pathology | Disease Progression | Magnetic Resonance Imaging | Aortic Valve Stenosis - complications | Biopsy | Fibrosis | Aged | Hypertrophy, Left Ventricular - physiopathology | Hypertrophy, Left Ventricular - diagnostic imaging | Usage | Magnetic resonance imaging | Aortic valve stenosis | Cardiac patients | Research | Diagnosis | Health aspects | cTnI, cardiac troponin I | ECV, extracellular volume | IQR, interquartile range | LVH, left ventricular hypertrophy | LV, left ventricular | LGE, late gadolinium enhancement | AVR, aortic valve replacement | BNP, brain natriuretic peptide | ECG, electrocardiogram | CMR, cardiac magnetic resonance | iECV, indexed extracellular volume
Journal Article
Epigenetics, ISSN 1559-2294, 05/2015, Volume 10, Issue 5, pp. 418 - 430
Pharmacological histone deacetylase (HDAC) inhibitors attenuate pathological cardiac remodeling and hypertrophic gene expression; yet, the direct histone... 
HDAC inhibitor | cardiac hypertrophy | chromatin | next generation sequencing | epigenetics | histone acetylation | Cardiac hypertrophy | Epigenetics | Chromatin | Histone acetylation | Next generation sequencing | Icam1, Intercellular adhesion molecule 1 | C-t, threshold cycle number | Il21r, Interleukin-21 receptor | SEM, Standard Error of the Mean | ADVANCED HEART-FAILURE | BW, Body Weight | GENETICS & HEREDITY | NF-KAPPA-B | HYPERTENSIVE-RATS | Cxcl10, Chemokine (C-X-C Motif) ligand 10 | TRANSCRIPTION START SITES | MACs, Model-based Analysis of ChIP-seq | Traf3, TNF receptor-associated factor 3 | BNP, Brain natriuretic peptide | ChIP, Chromatin Immunoprecipitation | BIOCHEMISTRY & MOLECULAR BIOLOGY | NGS, Next Generation Sequencing | CROSS-TALK | Vcam1, Vascular cell adhesion molecule 1 | HUMAN GENOME | ANP, Atrial natriuretic peptide | CLASS-I | FS, Fractional Shortening | ENCODE, Encyclopedia of DNA Elements Consortium | LVDd, Left Ventricular Diastolic Dimension | NF kappa B, Nuclear factor of kappa light polypeptide gene enhancer in B-cells | UTR, Untranslated region | LV, Left Ventricle | alpha/beta MHC, Alpha/Beta myosin heavy chain | LVH, Left Ventricle Hypertrophy | cDNA, complementary DNA | TF, transcription factor | Serca2a, Sarcoplasmic reticulum Ca2+ ATPase | TSS, Transcription Start Site | Il6ra, Interleukin-6 receptor | HISTONE H3 ACETYLATION | FDR, False Discovery Rate | NES, normalized enrichment score | TAC, Transverse Aortic Constriction | PRESSURE-OVERLOAD | GAIIx, Genome Analyzer IIx | HDAC, Histone deacetylase | TAC veh, TAC vehicle | TSA, Trichostatin A | Ticam2, Toll-like receptor adaptor molecule 2 | EXPRESSION | TL, Tibia Length | Mice, Inbred C57BL | Histone Deacetylases - metabolism | Male | NF-kappa B - metabolism | Gene Expression Regulation - drug effects | Acetylation - drug effects | Animals | Aorta - surgery | Myocardium - metabolism | Cardiomegaly - surgery | Histone Deacetylase Inhibitors - pharmacology | Histones - metabolism | Cardiomegaly - genetics | Hydroxamic Acids - pharmacology | Cardiomegaly - metabolism
Journal Article
JACC: Cardiovascular Interventions, ISSN 1936-8798, 2014, Volume 7, Issue 6, pp. 662 - 673
Journal Article
Cardiovascular Pathology, ISSN 1054-8807, 2015, Volume 25, Issue 2, pp. 103 - 112
Abstract Mitochondrial (mt) DNA depletion and oxidative mtDNA damage have been implicated in the process of pathological cardiac remodeling. Whether these... 
Pathology | Mitochondrial cardiomyopathy | Oxidative stress | mtDNA depletion | Mitochondrial biogenesis | Cardiac remodeling | Myocardial hypertrophy | TARGET | CARDIAC & CARDIOVASCULAR SYSTEMS | CARDIOMYOPATHY | TRANSCRIPTION | INDUCTION | PATHOLOGY | PENETRANCE | FAILING HEART | DISEASE | GROWTH | CONTRIBUTES | RIGHT-VENTRICULAR HYPERTROPHY | Microscopy, Electron, Transmission | DNA, Mitochondrial - metabolism | Humans | Middle Aged | Oxidative Stress - physiology | Laser Capture Microdissection | Male | Heart Failure - pathology | Ventricular Remodeling - physiology | Blotting, Western | Organelle Biogenesis | Hypertrophy, Left Ventricular - pathology | Myocardial Ischemia - complications | Adult | Female | Aged | Heart Failure - etiology | Real-Time Polymerase Chain Reaction | Heart failure | Proteins | Biosynthesis | Mitochondrial DNA | Ischemia | Hypertrophy | PGC-1α, peroxisome proliferator-activated receptor gamma coactivator 1 alpha, PPARGC1A | SDS-PAGE, sodiumdodecylsulphate–polyacrylamide gel electrophoresis | PPARα, peroxisome proliferator-activated receptor alpha PPARA | PVDF, polyvinylidene fluoride | NRF1, nuclear respiratory factor 1 | OXPHOS, oxidative phosphorylation | CAT, catalase | HF, heart failure | SOD2, superoxide dismutase 2 | mtDNA, mitochondrial DNA | GPx, glutathione peroxidase | LCM, laser capture microdissection | COX, cytochrome c oxidase | HPRT1, hypoxanthine phosphoribosyltransferase 1 | MIC, mitochondrial cardiomyopathies | NPPA, natriuretic peptide A | POLG, polymerase (DNA directed) gamma | SDH, succinate dehydrogenase | TEM, transmission electron microscopy | LV, left ventricular | DNPH, 2,4-dinitrophenylhydrazine | DNP, antidinitrophenyl | NADPH, nicotinamide adenine dinucleotide phosphate | ERRα, estrogen-related receptor alpha ESRRA | MDA, malondialdehyde | TFAM, mitochondrial transcription factor A | Original
Journal Article
Journal of the American College of Cardiology, ISSN 0735-1097, 02/2018, Volume 71, Issue 8, pp. 860 - 871
Left ventricular (LV) hypertrophy, a key process in human cardiac disease, results from cellular (hypertrophy) and extracellular matrix expansion (interstitial... 
left ventricular hypertrophy | fibrosis | aortic stenosis | CARDIAC & CARDIOVASCULAR SYSTEMS | CARDIOVASCULAR MAGNETIC-RESONANCE | DIASTOLIC FUNCTION | MASS REGRESSION | DISEASE | CMR | EXTRACELLULAR VOLUME | PROGNOSTIC-SIGNIFICANCE | LEFT-VENTRICULAR HYPERTROPHY | Prospective Studies | Follow-Up Studies | Heart Valve Prosthesis Implantation - trends | Humans | Middle Aged | Male | Ventricular Remodeling - physiology | Aortic Valve Stenosis - diagnostic imaging | Multimodal Imaging - methods | Aged, 80 and over | Female | Aged | Aortic Valve Stenosis - surgery | Cohort Studies | Care and treatment | Aortic valve stenosis | Natriuretic peptides | Heart | Stenosis | Gadolinium | Reduction | Calcium-binding protein | Electrocardiography | Aorta | Extracellular matrix | Bioindicators | Rheumatic heart disease | Heart diseases | Heart failure | Brain natriuretic peptide | Echocardiography | Magnetic resonance | Patients | Coronary artery disease | Troponin T | Concentration (composition) | Troponin | Biopsy | Fibrosis | Biomarkers | Cell size | Ventricle | Plastics | Mercury | Aortic valve | Cellular structure | Hypertrophy | Structure-function relationships | LVM, left ventricular mass | LVEF, left ventricular ejection fraction | 6MWT, 6-min walk test | LVMI, left ventricular mass index | ECV, extracellular volume fraction | LVH, left ventricular hypertrophy | LV, left ventricular | AS, aortic stenosis | LGE, late gadolinium enhancement | CMR, cardiovascular magnetic resonance | AVR, aortic valve replacement | hsTnT, high-sensitivity troponin T | NT-proBNP, N-terminal pro–B-type natriuretic peptide | NYHA, New York Heart Association
Journal Article
American Journal of Hypertension, ISSN 0895-7061, 06/2017, Volume 30, Issue 6, pp. 617 - 623
Journal Article