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1. Full Text Targeting of the pulmonary capillary vascular niche promotes lung alveolar repair and ameliorates fibrosis
by Cao, Zhongwei and Lis, Raphael and Ginsberg, Michael and Chavez, Deebly and Shido, Koji and Rabbany, Sina Y and Fong, Guo-Hua and Sakmar, Thomas P and Rafii, Shahin and Ding, Bi-Sen
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
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2. Full Text Tubastatin ameliorates pulmonary fibrosis by targeting the TGFβ-PI3K-Akt pathway
by Saito, Shigeki and Zhuang, Yan and Shan, Bin and Danchuk, Svitlana and Luo, Fayong and Korfei, Martina and Guenther, Andreas and Lasky, Joseph A
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
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3. Full Text Fluorofenidone attenuates pulmonary inflammation and fibrosis via inhibiting the activation of NALP3 inflammasome and IL‐1β/IL‐1R1/MyD88/NF‐κB pathway
by Song, Cheng and He, Lujuan and Zhang, Jin and Ma, Hong and Yuan, Xiangning and Hu, Gaoyun and Tao, Lijian and Zhang, Jian and Meng, Jie
Journal of Cellular and Molecular Medicine, ISSN 1582-1838, 11/2016, Volume 20, Issue 11, pp. 2064 - 2077
Interleukin (IL)‐1β plays an important role in the pathogenesis of idiopathic pulmonary fibrosis. The production of IL‐1β is dependent upon... 
fluorofenidone | IL‐1β/IL‐1R1/MyD88/NF‐κB pathway | NALP3 inflammasome | pulmonary fibrosis | IL-1β/IL-1R1/MyD88/NF-κB pathway | Inflammasomes - metabolism | Reactive Oxygen Species - metabolism | Humans | Actins - metabolism | Caspase 1 - metabolism | Male | NF-kappa B - metabolism | Receptors, Interleukin - metabolism | Bleomycin | Interleukin-1beta - metabolism | Pneumonia - chemically induced | Chemokine CCL2 - metabolism | Lung - metabolism | Pulmonary Fibrosis - metabolism | Interleukin-6 - metabolism | Lung - pathology | Collagen Type I - metabolism | NLR Family, Pyrin Domain-Containing 3 Protein - metabolism | Pulmonary Fibrosis - complications | Mice, Inbred C57BL | Pulmonary Fibrosis - pathology | Myeloid Differentiation Factor 88 | Down-Regulation - drug effects | Fibronectins - metabolism | Animals | Pneumonia - drug therapy | Signal Transduction - drug effects | Uric Acid - pharmacology | Lung - drug effects | Pneumonia - complications | Pyridones - therapeutic use | Pulmonary Fibrosis - drug therapy | Pneumonia - metabolism | Pyridones - pharmacology | Peroxidase - metabolism | IL‐1β | NF‐κB pathway | IL‐1R1 | Original | MyD88
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4. Full Text Caveolin-1: A critical regulator of lung fibrosis in idiopathic pulmonary fibrosis
by Xiao, Mei Wang and Zhang, Yingze and Hong, Pyo Kim and Zhou, Zhihong and Feghali-Bostwick, Carol A and Liu, Fang and Ifedigbo, Emeka and Xu, Xiaohui and Oury, Tim D and Kaminski, Naftali and Choi, Augustine M.K
Journal of Experimental Medicine, ISSN 0022-1007, 12/2006, Volume 203, Issue 13, pp. 2895 - 2906
Idiopathic pulmonary fibrosis (IPF) is a progressive chronic disorder characterized by activation of fibroblasts and overproduction of extracellular matrix... 
PATHOGENESIS | MEDICINE, RESEARCH & EXPERIMENTAL | LOCALIZATION | ACTIVATION | PATHWAY | ANTIFIBROTIC AGENT | IMMUNOLOGY | EXPRESSION | FAMILY | RNA, Small Interfering - genetics | Phosphorylation | Epithelial Cells - metabolism | Mitogen-Activated Protein Kinase 8 - antagonists & inhibitors | Epithelial Cells - drug effects | Humans | Transforming Growth Factor beta1 - metabolism | Actins - metabolism | Extracellular Matrix - metabolism | JNK Mitogen-Activated Protein Kinases - metabolism | Transfection | Mitogen-Activated Protein Kinase 8 - genetics | Lung - metabolism | Pulmonary Fibrosis - metabolism | Transforming Growth Factor beta1 - pharmacology | Fibroblasts - metabolism | Gene Expression | Lung - pathology | Collagen Type I - metabolism | JNK Mitogen-Activated Protein Kinases - antagonists & inhibitors | Hydroxyproline - metabolism | Mice, Inbred C57BL | Mitogen-Activated Protein Kinase 8 - metabolism | Smad2 Protein - metabolism | Caveolin 1 - genetics | Fibronectins - metabolism | Mice, Knockout | Caveolin 1 - metabolism | Animals | Fibroblasts - drug effects | Fibrosis | Pulmonary Fibrosis - physiopathology | Pulmonary Fibrosis - chemically induced | Bleomycin - pharmacology | Mice | Caveolin 1 - physiology
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5. Full Text Chk1 is dispensable for G2 arrest in response to sustained DNA damage when the ATM p53 p21 pathway is functional
by Lossaint, G and Besnard, E and Fisher, D and Piette, J and Dulić, V
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
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6. Full Text Neutrophil extracellular traps promote differentiation and function of fibroblasts
by Chrysanthopoulou, Akrivi and Mitroulis, Ioannis and Apostolidou, Eirini and Arelaki, Stella and Mikroulis, Dimitrios and Konstantinidis, Theocharis and Sivridis, Efthimios and Koffa, Maria and Giatromanolaki, Alexandra and Boumpas, Dimitrios T and Ritis, Konstantinos and Kambas, Konstantinos
The Journal of Pathology, ISSN 0022-3417, 07/2014, Volume 233, Issue 3, pp. 294 - 307
Neutrophil activation by inflammatory stimuli and the release of extracellular chromatin structures (neutrophil extracellular traps – NETs) have been... 
fibrosis | neutrophil extracellular traps | fibroblast | autophagy | IL‐17 | IL-17 | DNA TRAPS | TALC | AIRWAY INFLAMMATION | INJURY | BLEOMYCIN | PATHOLOGY | PATHOGENESIS | ONCOLOGY | LUNG-DISEASE | CIGARETTE-SMOKE | PULMONARY-FIBROSIS | COPD | Chromatin - metabolism | Cell Proliferation | Cicatrix - immunology | Skin - metabolism | Coculture Techniques | Humans | Actins - metabolism | Neutrophil Infiltration | Autophagy | Myofibroblasts - metabolism | Cicatrix - metabolism | Lung - metabolism | Pulmonary Fibrosis - metabolism | Neutrophils - metabolism | Skin - pathology | Skin - immunology | Myofibroblasts - pathology | Lung - pathology | Neutrophil Activation | Neutrophils - drug effects | Cells, Cultured | Enzyme Inhibitors - pharmacology | Pulmonary Fibrosis - immunology | Pulmonary Fibrosis - pathology | Myofibroblasts - drug effects | Collagen - metabolism | Interleukin-17 - metabolism | Phenotype | Cell Differentiation - drug effects | Lung - drug effects | Paracrine Communication - drug effects | Fibrosis | Cicatrix - pathology | Connective Tissue Growth Factor - metabolism | Cell Movement | Peroxidase - metabolism | Glycosaminoglycans | Collagen | Histones | Anticoagulants (Medicine) | Silicates | Muscle proteins | Intermediate filament proteins | Smoking
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7. Full Text miR-21 mediates fibrogenic activation of pulmonary fibroblasts and lung fibrosis
by Liu, Gang and Friggeri, Arnaud and Yang, Yanping and Milosevic, Jadranka and Ding, Qiang and Thannickal, Victor J and Kaminski, Naftali and Abraham, Edward
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
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8. Full Text Bone marrow-derived progenitor cells in pulmonary fibrosis
by Hashimoto, Naozumi and Jin, Hong and Liu, Tianju and Chensue, Stephen W and Phan, Sem H
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
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9. Full Text Identification of an atypical monocyte and committed progenitor involved in fibrosis
by Satoh, Takashi and Nakagawa, Katsuhiro and Sugihara, Fuminori and Kuwahara, Ryusuke and Ashihara, Motooki and Yamane, Fumihiro and Minowa, Yosuke and Fukushima, Kiyoharu and Ebina, Isao and Yoshioka, Yoshichika and Kumanogoh, Atsushi and Akira, Shizuo
Nature, ISSN 0028-0836, 01/2017, Volume 541, Issue 7635, pp. 96 - 101
Monocytes and macrophages comprise a variety of subsets with diverse functions(1-5). It is thought that these cells play a crucial role in homeostasis of... 
HOMEOSTASIS | ORIGIN | BASOPHILS | MACROPHAGES | INFLAMMATION | MULTIDISCIPLINARY SCIENCES | RATHER | DIFFERENTIATION | TRANSCRIPTION FACTOR | POLARIZATION | HOST RESPONSES | Granulocytes - cytology | Granulocyte-Macrophage Progenitor Cells - cytology | Male | Monocytes - metabolism | Pulmonary Fibrosis - genetics | Adoptive Transfer | Antigens, CD - metabolism | Molecular Targeted Therapy - trends | Monocytes - transplantation | CCAAT-Enhancer-Binding Protein-beta - deficiency | Monocytes - pathology | Antigens, Ly - metabolism | Cell Differentiation | Granulocytes - metabolism | Monocytes - classification | Bleomycin - toxicity | Disease Models, Animal | Biomarkers - metabolism | CCAAT-Enhancer-Binding Protein-beta - genetics | Inflammation | Pulmonary Fibrosis - pathology | Cell Adhesion Molecules - metabolism | CCAAT-Enhancer-Binding Protein-beta - metabolism | Animals | Receptors, IgE - metabolism | Pulmonary Fibrosis - prevention & control | Pulmonary Fibrosis - chemically induced | Dendritic Cells - cytology | Mice | Granulocyte-Macrophage Progenitor Cells - metabolism | Scavenger Receptors, Class A - metabolism | Physiological aspects | Monocytes | Macrophages | Health aspects | Fibrosis | Leucocytes | Granulocytes | Disease | Pathogenesis | Bone marrow | Fibroblasts | Gene expression
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10. Full Text Dysregulated Lung Commensal Bacteria Drive Interleukin-17B Production to Promote Pulmonary Fibrosis through Their Outer Membrane Vesicles
by Yang, Daping and Chen, Jiangye and Chen, Xi and Wang, Jingjing and Wang, Honglin and Lou, Qi and Lou, Yunwei and Li, Li and Wu, Meng and Song, Xinyang and Qian, Youcun
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
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11. Full Text Lysocardiolipin acyltransferase regulates TGF-β mediated lung fibroblast differentiation
by Huang, Long Shuang and Jiang, Peiyue and Feghali-Bostwick, Carol and Reddy, Sekhar P and Garcia, Joe G.N and Natarajan, Viswanathan
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
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