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1. Full Text Assessment of Myocardial Fibrosis Using Multimodality Imaging in Severe Aortic Stenosis: Comparison With Histologic Fibrosis
by Park, Sung-Ji and Cho, Sung Woo and Kim, Sung Mok and Kim, Sung Mok and Ahn, Joonghyun and Carriere, Keumhee and Carriere, Keumhee and Jeong, Dong Seop and Jeong, Dong Seop and Lee, Sang-Chol and Lee, Sang-Chol and Park, Seung Woo and Choe, Yeon Hyeon and Choe, Yeon Hyeon and Park, Pyo Won and Park, Pyo Won and Oh, Jae K and Oh, Jae K
JACC: Cardiovascular Imaging, ISSN 1936-878X, 01/2019, Volume 12, Issue 1, pp. 109 - 119
Objectives: This study assessed diffuse myocardial fibrosis (MF) by cardiac magnetic resonance (CMR) imaging and speckle-tracking echocardiography (STE) in... 
global longitudinal strain | severe aortic stenosis | extracellular volume | myocardial fibrosis | CARDIAC & CARDIOVASCULAR SYSTEMS | QUANTIFICATION | PROGNOSTIC VALUE | DEFORMATION | RECOMMENDATIONS | MAGNETIC-RESONANCE | SPECKLE-TRACKING ECHOCARDIOGRAPHY | ASYMPTOMATIC PATIENTS | EXTRACELLULAR VOLUME FRACTION | ASSOCIATION | RADIOLOGY, NUCLEAR MEDICINE & MEDICAL IMAGING | Care and treatment | Usage | Echocardiography | Magnetic resonance imaging | Comparative analysis | Aortic valve stenosis
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2. Full Text The pathogenesis of cardiac fibrosis
by Kong, Ping and Christia, Panagiota and Frangogiannis, Nikolaos G
Cellular and Molecular Life Sciences, ISSN 1420-682X, 2/2014, Volume 71, Issue 4, pp. 549 - 574
Cardiac fibrosis is characterized by net accumulation of extracellular matrix proteins in the cardiac interstitium, and contributes to both systolic and... 
Biochemistry, general | Myofibroblast | Biomedicine general | Cell Biology | Life Sciences | Chemokine | Life Sciences, general | Angiotensin | TGF-β | Extracellular matrix | Mast cell | Cardiac remodeling | Macrophage | SMOOTH MUSCLE ACTIN | BIOCHEMISTRY & MOLECULAR BIOLOGY | MONOCYTE CHEMOATTRACTANT PROTEIN-1 | HEALING MYOCARDIAL INFARCTS | CELL BIOLOGY | TGF-beta | TUMOR-NECROSIS-FACTOR | GROWTH-FACTOR-BETA | MARROW-DERIVED CELLS | LISINOPRIL-MEDIATED REGRESSION | HUMAN HYPERTROPHIC CARDIOMYOPATHY | MATRIX-METALLOPROTEINASE ACTIVITY | HYPERTENSIVE HEART-DISEASE | Mast Cells - immunology | Myofibroblasts - pathology | Myocardium - immunology | Macrophages - pathology | Signal Transduction | Myofibroblasts - immunology | Fibrosis - complications | Humans | Myocardium - pathology | Heart Failure - pathology | Animals | Angiotensins - immunology | Mast Cells - pathology | Fibrosis - immunology | Fibrosis - pathology | Heart Failure - etiology | Macrophages - immunology | Cytokines - immunology | Proteins | Medical colleges | Proteases | Cardiac patients | Fibrosis | Growth factors | Cardiac arrhythmia | Matrix | Pathogenesis | Chemokines | chemokine | myofibroblast | cardiac remodeling | mast cell | angiotensin | macrophage | extracellular matrix
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3. Full Text Resolution of organ fibrosis
by Jun, Joon-Il and Lau, Lester F
Journal of Clinical Investigation, ISSN 0021-9738, 01/2018, Volume 128, Issue 1, pp. 97 - 107
Fibrosis is the excessive accumulation of extracellular matrix that often occurs as a wound healing response to repeated or chronic tissue injury, and may lead... 
MEDICINE, RESEARCH & EXPERIMENTAL | LUNG FIBROSIS | TO-MESENCHYMAL TRANSITION | HEPATIC STELLATE CELLS | MYOCARDIAL FIBROSIS | LIVER FIBROSIS | INTERSTITIAL FIBROSIS | TISSUE INHIBITOR | IDIOPATHIC PULMONARY-FIBROSIS | CELLULAR SENESCENCE | FIBROBLAST SENESCENCE | Development and progression | Health aspects | Fibrosis | Apoptosis | Senescence | Wound healing | Gallbladder diseases | Smooth muscle | Inflammation | Gene expression | Kinases | Hepatitis | Pulmonary fibrosis | Rodents | Gastroenterology | Fibroblasts | Extracellular matrix | Liver cirrhosis | Bile | Chronic illnesses
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4. Full Text The Biological Basis for Cardiac Repair After Myocardial Infarction: From Inflammation to Fibrosis
by Prabhu, Sumanth D and Frangogiannis, Nikolaos G
Circulation Research, ISSN 0009-7330, 06/2016, Volume 119, Issue 1, pp. 91 - 112
In adult mammals, massive sudden loss of cardiomyocytes after infarction overwhelms the limited regenerative capacity of the myocardium, resulting in the... 
myocytes, cardiac | ISCHEMIA/REPERFUSION INJURY | CARDIAC & CARDIOVASCULAR SYSTEMS | REGULATES FIBROBLAST PHENOTYPE | myocardial infarction | HEART-FAILURE | immune cells | chemokines | ISCHEMIA-REPERFUSION INJURY | TOLL-LIKE RECEPTOR-2 | PERCUTANEOUS CORONARY INTERVENTION | inflammation | MARROW-DERIVED CELLS | KILLER T-CELLS | MOBILITY GROUP BOX-1 | PERIPHERAL VASCULAR DISEASE | cytokines | fibrosis | HEMATOLOGY | NF-KAPPA-B | Inflammation - pathology | Regeneration | Inflammation - metabolism | Animals | Cell Proliferation | Myocytes, Cardiac - physiology | Humans | Myocardial Infarction - pathology | Fibrosis | Myocytes, Cardiac - metabolism | Myocardial Infarction - metabolism | Heart Failure | Immune Cells | Myocardial Infarction | Inflammation | Remodeling
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5. Full Text Fibrosis and Cardiac Arrhythmias
by de Jong, Sanne and van Veen, Toon A. B and van Rijen, Harold V. M and de Bakker, Jacques M. T
Journal of Cardiovascular Pharmacology, ISSN 0160-2446, 06/2011, Volume 57, Issue 6, pp. 630 - 638
In this review article about fibrosis and arrhythmias, we show that the amount of collagen, a normal element of the heart muscle, increases with age and in... 
collagen | fibrosis | arrhythmias | electrophysiology | GAP JUNCTIONAL CONDUCTANCE | CARDIAC & CARDIOVASCULAR SYSTEMS | IDIOPATHIC DILATED CARDIOMYOPATHY | CARDIOVASCULAR MAGNETIC-RESONANCE | VENTRICULAR-TACHYCARDIA | HEART-FAILURE | LATE GADOLINIUM ENHANCEMENT | HYPERTROPHIC CARDIOMYOPATHY | MYOCARDIAL FIBROSIS | DELAYED CONTRAST ENHANCEMENT | PHARMACOLOGY & PHARMACY | ALTERED CONNEXIN43 EXPRESSION | Cardiomyopathies - drug therapy | Arrhythmias, Cardiac - prevention & control | Heart Atria - pathology | Endomyocardial Fibrosis - etiology | Channelopathies - physiopathology | Humans | Tachycardia, Ventricular - etiology | Magnetic Resonance Imaging - methods | Cardiomyopathies - pathology | Arrhythmias, Cardiac - etiology | Cardiomyopathies - etiology | Cardiomyopathies - physiopathology | Animals | Tachycardia, Ventricular - diagnosis | Fibrosis | Aging | Endomyocardial Fibrosis - drug therapy | Arrhythmias, Cardiac - diagnosis | Endomyocardial Fibrosis - physiopathology | Heart Atria - physiopathology | Early Diagnosis
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6. Full Text Potential Therapeutic Targets for Cardiac Fibrosis: TGFβ, Angiotensin, Endothelin, CCN2, and PDGF, Partners in Fibroblast Activation
by Leask, Andrew
Circulation Research, ISSN 0009-7330, 06/2010, Volume 106, Issue 11, pp. 1675 - 1680
Fibrosis is one of the largest groups of diseases for which there is no therapy but is believed to occur because of a persistent tissue repair program. During... 
TGF | Endothelin | Scarring | PDGF | Fibrosis | CARDIAC & CARDIOVASCULAR SYSTEMS | scarring | GENE-REGULATION | FIBROTIC PHENOTYPE | MATRIX CONTRACTION | endothelin | GROWTH-FACTOR-BETA | MYOCARDIAL FIBROSIS | IN-VIVO | PERIPHERAL VASCULAR DISEASE | fibrosis | SMOOTH-MUSCLE-CELLS | DERMAL FIBROBLASTS | TGF beta | MICE LACKING SMAD3 | HEMATOLOGY | MYOFIBROBLAST DIFFERENTIATION
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7. Full Text Allogeneic Human Mesenchymal Stem Cells in Patients With Idiopathic Pulmonary Fibrosis via Intravenous Delivery (AETHER): A Phase I Safety Clinical Trial
by Glassberg, Marilyn K and Minkiewicz, Julia and Toonkel, Rebecca L and Simonet, Emmanuelle S and Rubio, Gustavo A and DiFede, Darcy and Shafazand, Shirin and Khan, Aisha and Pujol, Marietsy V and LaRussa, Vincent F and Lancaster, Lisa H and Rosen, Glenn D and Fishman, Joel and Mageto, Yolanda N and Mendizabal, Adam and Hare, Joshua M
Chest, ISSN 0012-3692, 05/2017, Volume 151, Issue 5, pp. 971 - 981
Background Despite Food and Drug Administration approval of 2 new drugs for idiopathic pulmonary fibrosis (IPF), curative therapies remain elusive and... 
idiopathic pulmonary fibrosis | safety trial | mesenchymal stem cells | bone marrow | MYOCARDIAL-INFARCTION | BONE-MARROW | INTERSTITIAL PNEUMONIA | RANDOMIZED-TRIAL | TRANSENDOCARDIAL INJECTION | RAT MODEL | ISCHEMIC CARDIOMYOPATHY | RESPIRATORY SYSTEM | DOUBLE-BLIND | STROMAL CELLS | MARROW PROGENITOR CELLS | CRITICAL CARE MEDICINE | Idiopathic Pulmonary Fibrosis - therapy | Carbon Monoxide | Humans | Middle Aged | Mortality | Male | Total Lung Capacity | Hospitalization | Pulmonary Embolism - epidemiology | Disease Progression | Transplantation, Homologous | Mesenchymal Stem Cell Transplantation - methods | Vital Capacity | Administration, Intravenous | Pulmonary Diffusing Capacity | Dyspnea | Female | Stroke - epidemiology | Aged | Idiopathic Pulmonary Fibrosis - physiopathology | Walk Test | Drugs | Pulmonary fibrosis | Stem cells | Development and progression | Diagnosis | Research | Licensing, certification and accreditation | Dlco, diffusing capacity of the lungs for carbon monoxide | MedDRA, Medical Dictionary for Regulatory Activities | 6-MWT, 6-min walk test | FDA, Food and Drug Administration | MSCs, mesenchymal stem cells | hMSCs, human mesenchymal stem cells | HRCT, high-resolution CT | IPF, idiopathic pulmonary fibrosis | Diffuse Lung Disease
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8. Full Text Fibroblast-specific TGF-β-Smad2/3 signaling underlies cardiac fibrosis
by Khalil, Hadi and Kanisicak, Onur and Prasad, Vikram and Correll, Robert N and Fu, Xing and Schips, Tobias and Vagnozzi, Ronald J and Liu, Ruijie and Huynh, Thanh and Lee, Se-Jin and Karch, Jason and Molkentin, Jeffery D
Journal of Clinical Investigation, ISSN 0021-9738, 10/2017, Volume 127, Issue 10, pp. 3770 - 3783
The master cytokine TGF-beta mediates tissue fibrosis associated with inflammation and tissue injury. TGF-beta induces fibroblast activation and... 
GENETIC MANIPULATION | MEDICINE, RESEARCH & EXPERIMENTAL | HYPERTROPHY | GROWTH-FACTOR-BETA | HEART-DISEASE | TGF-BETA | SMAD3 | MYOCARDIAL-INFARCTION | IN-VIVO | MYOFIBROBLAST DIFFERENTIATION | PROTECTS | Receptors, Transforming Growth Factor beta - genetics | Heart Diseases - metabolism | Male | Smad3 Protein - metabolism | Myofibroblasts - metabolism | Smad3 Protein - genetics | Gene Deletion | Myocardium - metabolism | Smad2 Protein - genetics | Protein-Serine-Threonine Kinases - metabolism | Myofibroblasts - pathology | Signal Transduction | Protein-Serine-Threonine Kinases - genetics | Smad2 Protein - metabolism | Mice, Transgenic | Myocardium - pathology | Organ Specificity | Myocytes, Cardiac - pathology | Animals | Transforming Growth Factor beta - genetics | Receptors, Transforming Growth Factor beta - metabolism | Fibrosis | Myocytes, Cardiac - metabolism | Mice | Transforming Growth Factor beta - metabolism | Heart Diseases - genetics | Heart Diseases - pathology | Transcription factors | Phosphorylation | Heart attacks | Disease | Homeostasis | Smad3 protein | Gene deletion | Kinases | Proteins | Clonal deletion | Smad2 protein | Rodents | Fibroblasts | Extracellular matrix | Heart diseases | Growth factors | Heart failure | Cytokines | Cardiomyocytes | Gene expression | Pressure | Latency | Adenoviruses | Genetic engineering | Apoptosis
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9. Full Text Prevention of cardiac dysfunction, kidney fibrosis and lipid metabolic alterations in l-NAME hypertensive rats by sinapic acid—Role of HMG-CoA reductase
by Silambarasan, Thangarasu and Manivannan, Jeganathan and Raja, Boobalan and Chatterjee, Suvro
European Journal of Pharmacology, ISSN 0014-2999, 04/2016, Volume 777, pp. 113 - 123
The present study was designed to evaluate the effect of sinapic acid, a bioactive phenolic acid on high blood pressure associated cardiac dysfunction, kidney... 
Sinapic acid | Oxidative stress | Kidney fibrosis | Cardiac dysfunction | Dyslipidemia | CHOLESTEROL | NITRIC-OXIDE SYNTHASE | NO INHIBITION | LOW-DENSITY-LIPOPROTEIN | MYOCARDIAL INFARCTED RATS | BLOOD-PRESSURE | HYPERTROPHY | PLASMA | CARDIOVASCULAR-DISEASE | PHARMACOLOGY & PHARMACY | Kidney - pathology | Rats, Wistar | Mitochondria, Liver - metabolism | Antioxidants - metabolism | Male | Lipid Peroxidation - drug effects | Lipoproteins - metabolism | Blood Pressure - drug effects | Acyl Coenzyme A - metabolism | Heart - physiopathology | NG-Nitroarginine Methyl Ester - pharmacology | Kidney - drug effects | Coumaric Acids - metabolism | Rats | Lipoproteins - blood | Mitochondria, Liver - enzymology | Hypertension - physiopathology | Acyl Coenzyme A - chemistry | Hypertension - metabolism | Mitochondria, Liver - drug effects | Organ Size - drug effects | Animals | Fibrosis | Heart - drug effects | Protein Conformation | Molecular Docking Simulation | Oxidative Stress - drug effects | Nitric Oxide - metabolism | Coumaric Acids - pharmacology | Metabolites
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10. Full Text Getting to the Heart of the Matter: New Insights Into Cardiac Fibrosis
by Leask, Andrew
Circulation Research, ISSN 0009-7330, 03/2015, Volume 116, Issue 7, pp. 1269 - 1276
Fibrotic diseases are a significant global burden for which there are limited treatment options. The effector cells of fibrosis are activated fibroblasts... 
platelet-derived growth factor | fibrosis | endothelins | cicatrix | TISSUE-GROWTH-FACTOR | PRESSURE-OVERLOAD | CARDIAC & CARDIOVASCULAR SYSTEMS | FACTOR-BETA | TGF-BETA | MYOCARDIAL-INFARCTION | ANGIOTENSIN-II | REMODELING FOLLOWING INFARCTION | ENDOTHELIN-RECEPTOR ANTAGONIST | PERIPHERAL VASCULAR DISEASE | SMOOTH-MUSCLE-CELLS | MICE LACKING SMAD3 | HEMATOLOGY | Models, Cardiovascular | Myofibroblasts - physiology | Angiotensin II Type 1 Receptor Blockers - therapeutic use | Humans | Hypoxia - etiology | Transforming Growth Factor beta - physiology | Rats | Myocardium - pathology | Arrhythmias, Cardiac - etiology | Molecular Targeted Therapy | Atrophy | Animals | Connective Tissue Growth Factor - physiology | Signal Transduction - drug effects | Fibrosis | Anti-Inflammatory Agents - therapeutic use | Cicatrix - pathology | Pyridones - therapeutic use | Endothelin-1 - physiology | Endothelin Receptor Antagonists - therapeutic use | Platelet-Derived Growth Factor - physiology | Angiotensin II - physiology
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