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Nature Medicine, ISSN 1078-8956, 02/2016, Volume 22, Issue 2, pp. 154 - 162
Although the lung can undergo self-repair after injury, fibrosis in chronically injured or diseased lungs can occur at the expense of regeneration. Here we... 
MEDICINE, RESEARCH & EXPERIMENTAL | STEM-CELLS | ANGIOGENESIS | MACROPHAGE REGULATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | NOTCH | SIGNALING PROMOTES | CELL BIOLOGY | TO-MESENCHYMAL TRANSITION | ENDOTHELIAL-CELLS | DISEASE | SMOOTH-MUSCLE-CELLS | DIFFERENTIATION | Antibiotics, Antineoplastic - toxicity | Receptors, Notch - metabolism | Humans | Calcium-Binding Proteins - antagonists & inhibitors | Capillaries - drug effects | Hydrochloric Acid - toxicity | Smad3 Protein - metabolism | Pulmonary Circulation - physiology | Intercellular Signaling Peptides and Proteins - metabolism | Pulmonary Artery - metabolism | Receptors, CXCR - metabolism | Serrate-Jagged Proteins | Lung Injury - metabolism | Lung - metabolism | Membrane Proteins - metabolism | Pulmonary Fibrosis - metabolism | Capillaries - metabolism | Endothelial Cells - physiology | Wnt Signaling Pathway | Bleomycin - toxicity | Fibroblasts - metabolism | Jagged-1 Protein | Calcium-Binding Proteins - metabolism | Lung - pathology | Endothelial Cells - metabolism | RNA, Small Interfering - pharmacology | Vascular Endothelial Growth Factor Receptor-1 - metabolism | Pulmonary Artery - drug effects | Lung - physiology | Regeneration - physiology | Macrophages - metabolism | Regeneration - drug effects | Animals | Membrane Proteins - antagonists & inhibitors | Smad3 Protein - drug effects | Fibroblasts - drug effects | Lung - drug effects | Fibrosis | Fluorescent Antibody Technique | Macrophages - drug effects | Mice | Pulmonary Circulation - drug effects | Oligopeptides - pharmacology | Receptors, CXCR - agonists | Endothelial Cells - drug effects | Physiological aspects | Regeneration (Biology) | Lung diseases | Blood vessels | Angiogenesis | Pulmonary fibrosis | Cellular biology
Journal Article
PLoS ONE, ISSN 1932-6203, 10/2017, Volume 12, Issue 10, p. e0186615
Background Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive and fatal disease. Histone deacetylase 6 (HDAC6) alters function and fate of various... 
EPITHELIAL-MESENCHYMAL TRANSITION | LUNG FIBROSIS | IN-VITRO | TGF-BETA | HISTONE DEACETYLASE INHIBITION | MULTIDISCIPLINARY SCIENCES | TUBULIN ACETYLATION | DISEASE | AUTOPHAGY | MYOFIBROBLAST DIFFERENTIATION | EXPRESSION | Idiopathic Pulmonary Fibrosis - genetics | Ribosomal Protein S6 Kinases - metabolism | TOR Serine-Threonine Kinases - metabolism | Humans | Middle Aged | Phosphoprotein Phosphatases - metabolism | Male | Phosphatidylinositol 3-Kinases - metabolism | Vascular Endothelial Growth Factor A - metabolism | RNA, Messenger - metabolism | Autophagy - drug effects | Idiopathic Pulmonary Fibrosis - metabolism | Mechanistic Target of Rapamycin Complex 1 | Autophagosomes - drug effects | Multiprotein Complexes - metabolism | Tubulin - metabolism | Bleomycin | Hypoxia-Inducible Factor 1, alpha Subunit - metabolism | Aged, 80 and over | Female | Indoles - pharmacology | Lung - metabolism | Phosphorylation - drug effects | Proto-Oncogene Proteins c-akt - metabolism | Hydroxamic Acids - pharmacology | Fibroblasts - metabolism | Lung - pathology | Collagen Type I - metabolism | Histone Deacetylases - genetics | Histone Deacetylase 6 | RNA, Messenger - genetics | Histone Deacetylases - metabolism | Nuclear Proteins - metabolism | Autophagosomes - metabolism | Mice, Knockout | Transforming Growth Factor beta - pharmacology | Animals | Signal Transduction - drug effects | Fibroblasts - drug effects | Idiopathic Pulmonary Fibrosis - pathology | Hydroxamic Acids - therapeutic use | Indoles - therapeutic use | Aged | Transforming Growth Factor beta - metabolism | Idiopathic Pulmonary Fibrosis - drug therapy | Histone deacetylase | Deregulation | Collagen (type I) | Phosphorylation | Disease | Mesenchyme | Pathogenesis | Critical care | AKT protein | Leucine | Kinases | Autophagy | Proteins | Fibroblasts | Vascular endothelial growth factor | Internal medicine | Lung diseases | Environmental health | 1-Phosphatidylinositol 3-kinase | Medicine | Pulmonary fibrosis | Inhibitors | Lungs | Lysine | Deacetylation | Collagen | Fibrosis | Mice | Protein phosphatase | Phagocytosis
Journal Article
Journal of Cellular and Molecular Medicine, ISSN 1582-1838, 11/2016, Volume 20, Issue 11, pp. 2064 - 2077
Journal Article
Journal of Experimental Medicine, ISSN 0022-1007, 12/2006, Volume 203, Issue 13, pp. 2895 - 2906
Journal Article
Oncogene, ISSN 0950-9232, 10/2011, Volume 30, Issue 41, pp. 4261 - 4274
In the presence of sustained DNA damage occurring in S-phase or G2, normal cells arrest before mitosis and eventually become senescent. The checkpoint kinases... 
cyclin B1 | ATM | Chk2 | G2-M checkpoint | cell cycle | GENOTOXIC STRESS | BIOCHEMISTRY & MOLECULAR BIOLOGY | MITOTIC CATASTROPHE | TRANSCRIPTIONAL REPRESSION | G CHECKPOINT | CELL BIOLOGY | GENOMIC INSTABILITY | RETINOBLASTOMA PROTEIN | ONCOLOGY | GENETICS & HEREDITY | P53-DEFICIENT CELLS | CELL-CYCLE EXIT | IONIZING-RADIATION | ATAXIA-TELANGIECTASIA | Protein Kinases - metabolism | G2 Phase Cell Cycle Checkpoints - physiology | Phosphorylation | Protein Kinases - genetics | Tumor Suppressor Proteins - antagonists & inhibitors | Humans | Immunoblotting | Male | Cyclin B1 - metabolism | Pyrones - pharmacology | Tumor Suppressor Protein p53 - genetics | Cell Cycle Proteins - antagonists & inhibitors | DNA-Binding Proteins - metabolism | Cyclin-Dependent Kinase Inhibitor p21 - genetics | G2 Phase Cell Cycle Checkpoints - drug effects | RNA Interference | Tumor Suppressor Proteins - genetics | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Cell Cycle Proteins - genetics | Cyclin-Dependent Kinase Inhibitor p21 - metabolism | Female | Antineoplastic Agents - pharmacology | Protein-Serine-Threonine Kinases - metabolism | Tumor Suppressor Proteins - metabolism | DNA-Binding Proteins - antagonists & inhibitors | HCT116 Cells | Cell Cycle Proteins - metabolism | Cells, Cultured | Protein-Serine-Threonine Kinases - genetics | Tumor Suppressor Protein p53 - metabolism | Cyclin B1 - genetics | Morpholines - pharmacology | Signal Transduction - genetics | Ataxia Telangiectasia Mutated Proteins | DNA-Binding Proteins - genetics | Piperazines - pharmacology | G2 Phase Cell Cycle Checkpoints - genetics | Signal Transduction - drug effects | Cell Line, Tumor | Checkpoint Kinase 2 | Bleomycin - pharmacology | Checkpoint Kinase 1 | Signal Transduction - physiology | DNA Damage | HeLa Cells | Cell division | Oxidative stress | Signal transduction | DNA damage | Cyclin-dependent kinases | Cell cycle | CHK2 protein | Epithelial cells | Mitosis | CHK1 protein | G2 phase | Genotoxicity | Osteosarcoma cells | p53 protein | Cyclin-dependent kinase | Chemotherapy | Fibroblasts | Cancer
Journal Article
The Journal of Pathology, ISSN 0022-3417, 07/2014, Volume 233, Issue 3, pp. 294 - 307
Journal Article
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 | PHOSPHATASE | MECHANISMS | GROWTH-FACTOR | IMMUNOLOGY | MYOFIBROBLAST DIFFERENTIATION | EXPRESSION | 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 | Brief Definitive Report
Journal Article
Journal of Clinical Investigation, ISSN 0021-9738, 01/2004, Volume 113, Issue 2, pp. 243 - 252
The origin of fibroblasts in pulmonary fibrosis is assumed to be intrapulmonary, but their extrapulmonary origin and especially derivation from bone marrow... 
MEDICINE, RESEARCH & EXPERIMENTAL | EPITHELIUM | PERIPHERAL-BLOOD FIBROCYTES | TELOMERASE ACTIVITY | GENE-EXPRESSION | STEM-CELL | ALVEOLAR MYOFIBROBLASTS | MICE | DIFFERENTIATE | FIBROBLASTS | TRANSPLANTATION
Journal Article
Nature, ISSN 0028-0836, 01/2017, Volume 541, Issue 7635, pp. 96 - 101
Journal Article
Immunity, ISSN 1074-7613, 03/2019, Volume 50, Issue 3, pp. 692 - 706.e7
Idiopathic pulmonary fibrosis (IPF) is a severe form of lung fibrosis with a high mortality rate. However, the etiology of IPF remains unknown. Here, we report... 
bleomycin-induced fibrosis | lung microbiota | outer membrane vesicles | interleukin-17B | Prevotella | idiopathic pulmonary fibrosis | Bacteroides | CELLS | BIOGENESIS | IL-17 | GUT | MICROBIOME | AIRWAY INFLAMMATION | RECEPTOR | BLEOMYCIN | MECHANISMS | IMMUNOLOGY | EXPRESSION | Tumor Necrosis Factor-alpha - metabolism | Lung - microbiology | Microbiota - physiology | Cytokines - metabolism | Mice, Inbred C57BL | Idiopathic Pulmonary Fibrosis - microbiology | Idiopathic Pulmonary Fibrosis - metabolism | Prevotella - metabolism | Bacteroides - metabolism | Interleukin-17 - metabolism | Inflammation - metabolism | Animals | Bacterial Outer Membrane Proteins - metabolism | Signal Transduction - physiology | Lung - metabolism | Mice | Toll-Like Receptors - metabolism | Myeloid Differentiation Factor 88 - metabolism | Neutrophils - metabolism | Disease Models, Animal | Broadway theater | Medical colleges | Pulmonary fibrosis | Interleukins | Microbiota (Symbiotic organisms) | Mortality | Development and progression | Respiratory tract diseases | Bacteria | Children | Health aspects | Cells | Commensals | Pathogenesis | Genes | Interleukin | Helper cells | Gram-positive bacteria | Lymphocytes T | Experiments | Microbiota | Vesicles | Bleomycin | Etiology | Toll-like receptors | Tumor necrosis factor-TNF | Statistical analysis | Cytokines | Lung diseases | Membrane vesicles | Inflammation | Tumor necrosis factor-α | Gene expression | Signaling | Depletion | Lungs | Antibiotics | Fibrosis | MyD88 protein | Software
Journal Article
Free Radical Biology and Medicine, ISSN 0891-5849, 11/2017, Volume 112, pp. 162 - 173
Lysocardiolipin acyltransferase (LYCAT), a cardiolipin remodeling enzyme, plays a key role in mitochondrial function and vascular development. We previously... 
Mitochondrial oxidative stress | LYCAT | TGF-β | Pulmonary fibrosis | Fibroblast differentiation | BIOCHEMISTRY & MOLECULAR BIOLOGY | TGF-beta | ENDOCRINOLOGY & METABOLISM | MITOCHONDRIAL DYSFUNCTION | IDIOPATHIC PULMONARY-FIBROSIS | DEFICIENCY CONFERS PROTECTION | EXPRESSION | ALCAT1 | CYCLE | RNA, Small Interfering - genetics | Oxidative Stress | Humans | Male | Pulmonary Fibrosis - genetics | Smad3 Protein - metabolism | Acyltransferases - metabolism | Acyltransferases - genetics | Myofibroblasts - metabolism | Smad3 Protein - genetics | Bleomycin | Smad2 Protein - genetics | Superoxides - metabolism | Cell Differentiation | Lung - metabolism | Pulmonary Fibrosis - metabolism | Fibroblasts - metabolism | Pyrazoles - pharmacology | Myofibroblasts - pathology | Promoter Regions, Genetic | Lung - pathology | NADPH Oxidase 4 - genetics | Mice, Inbred C57BL | Gene Expression Regulation | Smad2 Protein - metabolism | Mitochondria - metabolism | Pulmonary Fibrosis - pathology | Mitochondria - drug effects | Fibroblasts - pathology | Myofibroblasts - drug effects | Smad3 Protein - antagonists & inhibitors | Hydrogen Peroxide - metabolism | Transforming Growth Factor beta - pharmacology | NADPH Oxidase 4 - metabolism | Animals | Fibroblasts - drug effects | Lung - drug effects | Protein Binding | Pulmonary Fibrosis - chemically induced | Mice | Pyridines - pharmacology | Primary Cell Culture | RNA, Small Interfering - metabolism
Journal Article