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Journal of Experimental Medicine, ISSN 0022-1007, 08/2010, Volume 207, Issue 8, pp. 1589 - 1597
Uncontrolled extracellular matrix production by fibroblasts in response to tissue injury contributes to fibrotic diseases, such as idiopathic pulmonary... 
MEDICINE, RESEARCH & EXPERIMENTAL | RESPONSES | PHOSPHATASE | INJURY | TENSIN HOMOLOG | MECHANISMS | GROWTH-FACTOR | IMMUNOLOGY | MYOFIBROBLAST DIFFERENTIATION | EXPRESSION | CANCER | MICRORNA | Oligonucleotides - genetics | Pulmonary Fibrosis - therapy | Idiopathic Pulmonary Fibrosis - genetics | Gene Expression - drug effects | Gene Expression - genetics | Humans | Actins - metabolism | MicroRNAs - metabolism | Pulmonary Fibrosis - genetics | Idiopathic Pulmonary Fibrosis - metabolism | Actins - genetics | Antisense Elements (Genetics) - therapeutic use | Collagen - genetics | Lung - metabolism | Phosphorylation - drug effects | Smad7 Protein - genetics | Extracellular Matrix Proteins - metabolism | Transforming Growth Factor beta1 - pharmacology | Fibroblasts - metabolism | Smad7 Protein - metabolism | Cell Line | Lung - pathology | Extracellular Matrix Proteins - genetics | Mice, Inbred C57BL | Smad2 Protein - metabolism | Mice, Transgenic | Pulmonary Fibrosis - pathology | Transforming Growth Factor beta1 - genetics | Fibroblasts - pathology | Fibronectins - metabolism | Collagen - metabolism | Animals | Fibroblasts - drug effects | Antisense Elements (Genetics) - genetics | Idiopathic Pulmonary Fibrosis - pathology | Pulmonary Fibrosis - chemically induced | Bleomycin - pharmacology | Fibronectins - genetics | Mice | MicroRNAs - genetics | Index Medicus | Brief Definitive Report
Journal Article
American Journal of Physiology - Lung Cellular and Molecular Physiology, ISSN 1040-0605, 2015, Volume 308, Issue 4, pp. L344 - L357
Pathological fibrosis is driven by a feedback loop in which the fibrotic extracellular matrix is both a cause and consequence of fibroblast activation.... 
Plasminogen activator inhibitor 1 | Extracellular matrix | Mechanotransduction | Hippo | Idiopathic pulmonary fibrosis | LUNG | DOMAIN | PHYSIOLOGY | mechanotransduction | HIPPO PATHWAY | idiopathic pulmonary fibrosis | TRANSCRIPTIONAL COACTIVATOR | plasminogen activator inhibitor 1 | GROWTH-FACTOR-BETA | MECHANICAL MEMORY | MATRIX STIFFNESS | INHIBITION | RESPIRATORY SYSTEM | DIFFERENTIATION | IDIOPATHIC PULMONARY-FIBROSIS | extracellular matrix | NIH 3T3 Cells | Humans | Male | Intracellular Signaling Peptides and Proteins - metabolism | Pulmonary Fibrosis - genetics | Phosphoproteins - metabolism | Serpin E2 - biosynthesis | Gene Knockdown Techniques | Female | Lung - metabolism | Pulmonary Fibrosis - metabolism | Plasminogen Activator Inhibitor 1 - genetics | Intracellular Signaling Peptides and Proteins - genetics | Mechanotransduction, Cellular - genetics | Fibroblasts - metabolism | Lung - pathology | Pulmonary Fibrosis - pathology | Phosphoproteins - genetics | Fibroblasts - pathology | Plasminogen Activator Inhibitor 1 - biosynthesis | Serpin E2 - genetics | Animals | Transforming Growth Factor beta - genetics | Adaptor Proteins, Signal Transducing - genetics | Mice, Inbred NOD | Mice | Mutation | Adaptor Proteins, Signal Transducing - metabolism | Transforming Growth Factor beta - metabolism | Transcriptional coactivators | Fibroblasts | Genetic aspects | Pulmonary fibrosis | Health aspects | Oncogenes | Bone morphogenetic proteins | Fibrosis | Signal transduction | Pathology | Cellular biology | Protein expression | Biosynthesis | Physiology | Binding sites | Index Medicus | Call for Papers
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 1/2014, Volume 111, Issue 1, pp. 367 - 372
Journal Article
American Journal of Respiratory and Critical Care Medicine, ISSN 1073-449X, 07/2010, Volume 182, Issue 2, pp. 220 - 229
Journal Article
Clinical Immunology, ISSN 1521-6616, 2010, Volume 137, Issue 1, pp. 89 - 101
Abstract Activated macrophages have been characterized as M1 and M2 according to their inflammatory response pattern. Here we analyzed the M2 marker expression... 
Allergy and Immunology | M2 phenotype | Th2 cytokines | Pulmonary fibrosis | IL-1RA | CCL22 | Sarcoidosis | JAK/STAT pathway | CCL18 | Alveolar macrophages | CCL17 | INTERLEUKIN-1 RECEPTOR ANTAGONIST | CYTOKINE | IMMUNOLOGY | SYSTEMIC-SCLEROSIS | STAT3 ACTIVATION | INTERSTITIAL LUNG-DISEASES | MANNOSE RECEPTOR | GENE-EXPRESSION | TNF-ALPHA RELEASE | GROWTH-FACTOR | UP-REGULATION | Mannose-Binding Lectins - metabolism | Tumor Necrosis Factor-alpha - metabolism | Gene Expression - drug effects | Humans | Middle Aged | STAT Transcription Factors - metabolism | Interleukin 1 Receptor Antagonist Protein - genetics | Male | Monocytes - metabolism | Monocytes - immunology | Sarcoidosis, Pulmonary - diagnosis | Idiopathic Pulmonary Fibrosis - metabolism | Young Adult | Lectins, C-Type - metabolism | Signal Transduction - immunology | Interleukin-4 - pharmacology | Interleukin 1 Receptor Antagonist Protein - metabolism | Scleroderma, Systemic - complications | Aged, 80 and over | Adult | Female | Bronchoalveolar Lavage Fluid - cytology | Pulmonary Fibrosis - metabolism | Interleukin-8 - metabolism | Macrophages, Alveolar - immunology | Pulmonary Fibrosis - etiology | Sarcoidosis, Pulmonary - complications | Cytokines - metabolism | Macrophage Activation - immunology | Scleroderma, Systemic - metabolism | Pulmonary Fibrosis - immunology | Receptors, Cell Surface - metabolism | Idiopathic Pulmonary Fibrosis - immunology | Monocytes - drug effects | Signal Transduction - drug effects | Macrophages, Alveolar - drug effects | Sarcoidosis, Pulmonary - metabolism | Chemokines, CC - genetics | Aged | Macrophages, Alveolar - metabolism | Macrophage Activation - drug effects | Interleukin-10 - pharmacology | Chemokines, CC - metabolism | Respiratory tract diseases | Systemic scleroderma | Transforming growth factors | Macrophages | Scleroderma (Disease) | Index Medicus | Alveoli
Journal Article
Journal Article
Journal of Experimental Medicine, ISSN 0022-1007, 07/2011, Volume 208, Issue 7, pp. 1459 - 1471
Journal Article
Nature Medicine, ISSN 1078-8956, 11/2016, Volume 22, Issue 11, pp. 1285 - 1293
Successful recovery from lung injury requires the repair and regeneration of alveolar epithelial cells to restore the integrity of gas-exchanging regions... 
MEDICINE, RESEARCH & EXPERIMENTAL | STEM-CELLS | REGENERATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | LUNG INJURY | PROLIFERATION | CELL BIOLOGY | REPAIR | EPITHELIAL-CELLS | CAPILLARY VASCULAR NICHE | TOLL-LIKE RECEPTORS | II CELLS | EXPRESSION | Cell Self Renewal - immunology | Stem Cells - immunology | Antibiotics, Antineoplastic - toxicity | Cell Proliferation | Humans | Stem Cells - metabolism | Idiopathic Pulmonary Fibrosis - metabolism | Alveolar Epithelial Cells - immunology | Cell Self Renewal - genetics | Glucuronosyltransferase - genetics | Flow Cytometry | Organoids | Lung Injury - metabolism | Hyaluronan Synthases | Pulmonary Fibrosis - metabolism | Real-Time Polymerase Chain Reaction | Bleomycin - toxicity | Severity of Illness Index | Cell Line | Hydroxyproline - metabolism | Pulmonary Fibrosis - immunology | Pulmonary Surfactant-Associated Protein C - metabolism | Toll-Like Receptor 4 - genetics | Alveolar Epithelial Cells - metabolism | Pulmonary Fibrosis - pathology | Toll-Like Receptor 4 - immunology | Idiopathic Pulmonary Fibrosis - immunology | Immunity, Innate | Toll-Like Receptor 4 - metabolism | Mice, Knockout | Animals | Hyaluronic Acid - metabolism | Interleukin-6 - immunology | Idiopathic Pulmonary Fibrosis - pathology | Mice | Lung Injury - chemically induced | Lung Injury - immunology | Prevention | Toll-like receptors | Genetic aspects | Pulmonary fibrosis | Hyaluronic acid | Health aspects | Proteins | Surfactants | Rodents | Cells | Index Medicus
Journal Article
Journal of Clinical Investigation, ISSN 0021-9738, 09/2009, Volume 119, Issue 9, pp. 2550 - 2563
Uncontrolled activation of the coagulation cascade contributes to the pathophysiology of several conditions, including acute and chronic lung diseases.... 
MEDICINE, RESEARCH & EXPERIMENTAL | GROWTH-FACTOR-BETA | BLOOD-COAGULATION | THROMBUS FORMATION | GENE-EXPRESSION | IDIOPATHIC PULMONARY-FIBROSIS | PROTEASE-ACTIVATED RECEPTOR-1 | TISSUE FACTOR EXPRESSION | SUSCEPTIBILITY GENES | RESPIRATORY-DISTRESS-SYNDROME | BRONCHOALVEOLAR LAVAGE | Up-Regulation | Lung Injury - pathology | Factor Xa Inhibitors | Receptor, PAR-1 - metabolism | Humans | Middle Aged | Actins - metabolism | Male | Pulmonary Fibrosis - blood | Idiopathic Pulmonary Fibrosis - blood | RNA, Messenger - metabolism | Case-Control Studies | Idiopathic Pulmonary Fibrosis - metabolism | Idiopathic Pulmonary Fibrosis - etiology | Base Sequence | Lung Injury - metabolism | Adult | Female | Cell Differentiation | Pulmonary Fibrosis - metabolism | Receptors, Vitronectin - metabolism | Pulmonary Fibrosis - etiology | Bleomycin - toxicity | Fibroblasts - metabolism | Gene Expression | Factor Xa - genetics | Mice, Inbred C57BL | RNA, Messenger - genetics | Cells, Cultured | Pulmonary Fibrosis - pathology | Fibroblasts - pathology | Factor Xa - metabolism | Animals | Transforming Growth Factor beta - genetics | Models, Biological | Fibroblasts - drug effects | Idiopathic Pulmonary Fibrosis - pathology | Aged | Mice | Transforming Growth Factor beta - metabolism | Transforming growth factors | Lung diseases | Integrins | Index Medicus | Abridged Index Medicus
Journal Article