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Journal Article
Journal Article
PloS one, ISSN 1932-6203, 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
Cardiovascular diabetology, ISSN 1475-2840, 2012, Volume 11, Issue 1, pp. 73 - 73
Background: Alpha-lipoic acid (ALA), a naturally occurring compound, exerts powerful protective effects in various cardiovascular disease models. However, its... 
Alpha-Lipoic acid | Mitochondrial oxidative stress | Cardiac fibrosis | Extracellular matrix remodeling | APOPTOSIS | CARDIAC & CARDIOVASCULAR SYSTEMS | METALLOTHIONEIN | KINASE | RATS | FIBROBLASTS | HEART | PATHOGENESIS | OVEREXPRESSION | ATTENUATION | ENDOCRINOLOGY & METABOLISM | Diabetes Mellitus, Experimental - drug therapy | Phosphorylation | Diabetic Cardiomyopathies - metabolism | Mitochondria, Heart - metabolism | Diabetic Cardiomyopathies - etiology | Rats, Wistar | Actins - metabolism | Extracellular Matrix - metabolism | Male | Mitochondria, Heart - drug effects | Diabetic Cardiomyopathies - physiopathology | Collagen Type II - metabolism | Myofibroblasts - metabolism | Tissue Inhibitor of Metalloproteinase-2 - metabolism | Cardiac Catheterization | Myocardium - metabolism | Gelatinases - metabolism | Diabetic Cardiomyopathies - prevention & control | Diabetes Mellitus, Experimental - complications | Diabetes Mellitus, Experimental - metabolism | Diabetes Mellitus, Experimental - physiopathology | Myofibroblasts - pathology | Collagen Type I - metabolism | Matrix Metalloproteinase 2 - metabolism | Extracellular Matrix - drug effects | Ventricular Function, Left - drug effects | Rats | Myocardium - pathology | Thioctic Acid - pharmacology | Cardiotonic Agents - pharmacology | Myofibroblasts - drug effects | Blotting, Western | Enzyme Precursors - metabolism | Animals | Signal Transduction - drug effects | Cell Differentiation - drug effects | Fibrosis | Diabetes Mellitus, Experimental - pathology | Diabetic Cardiomyopathies - pathology | Enzyme Activation | Oxidative Stress - drug effects | Spectrophotometry | Transforming Growth Factor beta - metabolism | Ventricular Remodeling - drug effects | Mitogen-Activated Protein Kinases - metabolism | Proteins | Medical research | Cardiovascular disease | Diabetes | Rodents | Metabolic disorders
Journal Article
Proceedings of the National Academy of Sciences - PNAS, ISSN 1091-6490, 2013, Volume 110, Issue 6, pp. 2324 - 2329
In many organs, myofibroblasts play a major role in the scarring process in response to injury. In liver fibrogenesis, hepatic stellate cells (HSCs) are... 
Phenotypes | Hepatocytes | Epithelial cells | Liver | Fibrosis | Cell lines | Antibodies | Hepatic stellate cells | Myofibroblasts | Liver cells | Epithelial-mesenchymal transition | Alpha-smooth muscle actin | Glisson's capsule | Podoplanin | alpha-smooth muscle actin | PATHWAYS | ACID | RAT | MULTIDISCIPLINARY SCIENCES | MOUSE | RECEPTOR | POPULATIONS | podoplanin | SMOOTH-MUSCLE | fibrosis | LINEAGE | Liver - pathology | WT1 Proteins - metabolism | Membrane Glycoproteins - metabolism | Hepatic Stellate Cells - metabolism | RNA, Messenger - metabolism | Liver - injuries | Myofibroblasts - metabolism | Biliary Tract - metabolism | Cell Transdifferentiation - drug effects | Liver Cirrhosis - metabolism | Chemical and Drug Induced Liver Injury - pathology | WT1 Proteins - genetics | Hepatic Stellate Cells - pathology | Liver Cirrhosis - etiology | Myofibroblasts - pathology | Epithelium - pathology | Gene Expression | Liver Regeneration | Epithelium - metabolism | Signal Transduction | Liver - metabolism | RNA, Messenger - genetics | Cells, Cultured | Mice, Transgenic | Chemical and Drug Induced Liver Injury - genetics | Carbon Tetrachloride - toxicity | Biliary Tract - pathology | Nerve Tissue Proteins - metabolism | Cell Lineage | Transforming Growth Factor beta - pharmacology | Animals | Chemical and Drug Induced Liver Injury - metabolism | Liver Cirrhosis - pathology | Mesoderm - metabolism | Mice | Mesoderm - pathology | Transforming Growth Factor beta - metabolism | Biological Sciences
Journal Article
Gastroenterology (New York, N.Y. 1943), ISSN 0016-5085, 2012, Volume 142, Issue 4, pp. 938 - 946
Background & Aims The pathogenesis of liver fibrosis involves activation of hepatic stellate cells, which is associated with depletion of intracellular lipid... 
Gastroenterology and Hepatology | Inflammation | Myofibroblasts | Energy Depletion | Mouse Model | RAT-LIVER | FIBROSIS | PATHWAY | DISEASE | MECHANISMS | RETINOL | GASTROENTEROLOGY & HEPATOLOGY | Liver - pathology | Kidney - pathology | Microtubule-Associated Proteins - genetics | Microtubule-Associated Proteins - metabolism | Carbon Tetrachloride | Humans | Hepatic Stellate Cells - metabolism | Autophagy - drug effects | Idiopathic Pulmonary Fibrosis - metabolism | Kidney - metabolism | Epoxy Compounds - pharmacology | Liver - drug effects | RNA Interference | Adenosine Triphosphate - metabolism | Liver Cirrhosis, Experimental - pathology | Lung - metabolism | Autophagy - genetics | Microtubule-Associated Proteins - deficiency | Hepatic Stellate Cells - pathology | Fibroblasts - metabolism | Hepatic Stellate Cells - drug effects | Cell Line | Lung - pathology | Oleic Acid - metabolism | Adenine - analogs & derivatives | Liver - metabolism | Mice, Inbred C57BL | Adenine - pharmacology | Liver Cirrhosis, Experimental - genetics | Fibroblasts - pathology | Mice, Knockout | Thioacetamide | Autophagy-Related Protein 7 | Animals | Autophagy-Related Protein 5 | Energy Metabolism | Fibroblasts - drug effects | Liver Cirrhosis, Experimental - chemically induced | Lipid Metabolism - drug effects | Idiopathic Pulmonary Fibrosis - pathology | Mice | Liver Cirrhosis, Experimental - metabolism | Phosphates | Medical colleges | Neurosciences | Platelet-derived growth factor | Liver diseases | Albumin | Lipids | Muscle proteins | Fatty acids | Cells | Monosaccharides | Unsaturated fatty acids | Monounsaturated fatty acids | Actin | Analysis | Intermediate filament proteins | Sugars
Journal Article
Proceedings of the National Academy of Sciences - PNAS, ISSN 1091-6490, 2014, Volume 111, Issue 41, pp. 14776 - 14781
Prostate cancer (PC) is a slowly progressing malignancy that often responds to androgen ablation or chemotherapy by becoming more aggressive, acquiring a... 
Androgens | Messenger RNA | Castration | B lymphocytes | Fibroblasts | Hypoxia | Myofibroblasts | Prostate cancer | Tumors | Cancer | Cancer-associated fibroblasts | Inflammation | Tumor microenvironment | cancer-associated fibroblasts | cancer | tumor microenvironment | inflammation | CELLS | ACTIVATION | METASTASIS | MULTIDISCIPLINARY SCIENCES | PHENOTYPE | PROLIFERATION | MECHANISMS | FIBROBLASTS | DIFFERENTIATION | HIF-1-ALPHA | Prostatic Neoplasms - metabolism | Adenocarcinoma - pathology | Humans | Receptors, Tumor Necrosis Factor, Member 25 - metabolism | Male | Prostate - metabolism | Prostatic Neoplasms, Castration-Resistant - pathology | Hypoxia - metabolism | Myofibroblasts - metabolism | Prostate - pathology | Adenocarcinoma - metabolism | Hypoxia-Inducible Factor 1, alpha Subunit - metabolism | Prostate - drug effects | Phosphodiesterase 5 Inhibitors - pharmacology | Myofibroblasts - pathology | Prostatic Neoplasms - pathology | Mice, Transgenic | Myofibroblasts - drug effects | Prostatic Neoplasms, Castration-Resistant - metabolism | Disease Progression | Animals | Androgens - pharmacology | Signal Transduction - drug effects | Hypoxia - pathology | Chemokine CXCL13 - metabolism | Transforming Growth Factor beta - metabolism | Connective Tissue Growth Factor - metabolism | Insulin-Like Growth Factor I - metabolism | Oncology, Experimental | Physiological aspects | Genetic research | Development and progression | Genetic aspects | Research | Gene expression | Health aspects | Biological Sciences
Journal Article
Human Pathology, ISSN 0046-8177, 2013, Volume 44, Issue 2, pp. 189 - 198
Journal Article
The Journal of pathology, ISSN 0022-3417, 2014, Volume 233, Issue 3, pp. 294 - 307
Journal Article
Cell Cycle, ISSN 1538-4101, 2014, Volume 11, Issue 16, pp. 3019 - 3035
.... As a consequence, Cav-1-low CAFs generate nutrients (such as L-lactate) and chemical building blocks that fuel mitochondrial metabolism and the anabolic growth of adjacent breast cancer cells... 
autophagy | paracrine signaling | myofibroblast | cancer associated fibroblast | the field effect | cancer metabolism | "Pied-Piper of Hamelin" | mitophagy | autocrine signaling | tumor stroma | TGF beta | aerobic glycolysis | oxidative stress | Binding | Proteins | Landes | Calcium | Bioscience | Biology | Cell | Cycle | Cancer | Organogenesis | Oxidative stress | Autocrine signaling | Myofibroblast | Tumor stroma | Paracrine signaling | Cancer associated fibroblast | Mitophagy | Autophagy | Cancer metabolism | The field effect | Aerobic glycolysis | Pied-Piper of Hamelin | SMOOTH MUSCLE ACTIN | TGF- beta | METASTASIS | CELL BIOLOGY | BREAST-CANCER | CAVEOLIN-1 EXPRESSION | EPITHELIAL-CELLS | MICROENVIRONMENT | TRANSFORMING GROWTH-FACTOR-BETA-1 | Immunohistochemistry | Receptors, Transforming Growth Factor beta - genetics | Oxidative Stress | Stromal Cells - pathology | Coculture Techniques | Humans | Gene Expression Regulation, Neoplastic | Tumor Microenvironment | Breast Neoplasms - metabolism | Cellular Reprogramming | Mitochondria - genetics | Cell Transformation, Neoplastic - genetics | Female | Protein-Serine-Threonine Kinases - metabolism | Fibroblasts - metabolism | Autocrine Communication | Paracrine Communication | Lactic Acid - metabolism | Stromal Cells - metabolism | Oxidative Phosphorylation | Protein-Serine-Threonine Kinases - genetics | Caveolin 1 - genetics | Mitochondria - metabolism | Mitochondria - pathology | Fibroblasts - pathology | Cell Transformation, Neoplastic - metabolism | Caveolin 1 - metabolism | Gene Expression Regulation, Enzymologic | Xenograft Model Antitumor Assays | Animals | Breast Neoplasms - genetics | Transforming Growth Factor beta - genetics | Receptors, Transforming Growth Factor beta - metabolism | Breast Neoplasms - pathology | Mice, Nude | Cell Line, Tumor | Glycolysis | Ligands | Mice | Neovascularization, Pathologic - metabolism | Transforming Growth Factor beta - metabolism | Report
Journal Article
Proceedings of the National Academy of Sciences - PNAS, ISSN 1091-6490, 2014, Volume 111, Issue 32, pp. E3297 - E3305
Journal Article