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International Journal of Molecular Sciences, ISSN 1661-6596, 01/2014, Volume 15, Issue 1, pp. 605 - 628
Journal Article
Journal of Cellular and Molecular Medicine, ISSN 1582-1838, 08/2017, Volume 21, Issue 8, pp. 1545 - 1554
Fibrosis in animal models and human diseases is associated with aberrant activation of the Wnt/β‐catenin pathway. Despite extensive research efforts, effective... 
Smad2/3 | myofibroblast proliferation | pulmonary fibrosis | Wnt/β‐catenin | Wnt/β-catenin | MEDICINE, RESEARCH & EXPERIMENTAL | TGF-BETA | MECHANISMS | BETA-CATENIN | PROTEIN CBP | CELL BIOLOGY | EPITHELIAL-MESENCHYMAL TRANSITION | PATHOGENESIS | INHIBITION | PATHWAY | Wnt/beta-catenin | IDIOPATHIC PULMONARY-FIBROSIS | PROMOTE | Cell Proliferation | Cadherins - metabolism | Vimentin - metabolism | Humans | Transforming Growth Factor beta1 - metabolism | Actins - metabolism | Smad3 Protein - metabolism | Wnt Proteins - metabolism | Actins - genetics | Myofibroblasts - metabolism | Smad3 Protein - genetics | Collagen Type I - genetics | Wnt Proteins - genetics | Vimentin - genetics | Smad2 Protein - genetics | Epithelial-Mesenchymal Transition | Cadherins - genetics | Fibroblasts - metabolism | A549 Cells | Cell Line | Myofibroblasts - pathology | Collagen Type I - metabolism | Signal Transduction | Gene Expression Regulation | Smad2 Protein - metabolism | Rats | Transforming Growth Factor beta1 - genetics | Fibroblasts - pathology | Rats, Sprague-Dawley | beta Catenin - metabolism | beta Catenin - genetics | Animals | Fibrosis | Vimentin | Animal models | Collagen (type I) | Wnt protein | Mesenchyme | Pathogenesis | Transforming growth factor-b | Activation | Proteins | β-catenin | Signal transduction | Molecular modelling | Lungs | Smad2 protein | Effectors | Fibroblasts | Extracellular matrix | Autocrine signalling | Aberration | Smad2 | β‐catenin | Wnt | Original
Journal Article
Journal Article
Journal of Cellular and Molecular Medicine, ISSN 1582-1838, 08/2016, Volume 20, Issue 8, pp. 1542 - 1549
Recent studies have suggested that platelet‐rich plasma (PRP) injections are an effective way to retard intervertebral disc degeneration, but the mechanism of... 
intervertebral disc degeneration | platelet‐rich plasma | TGF‐β1/Smad2/3 | rabbit | nucleus pulpous | TGF-β1/Smad2/3 | platelet-rich plasma | Immunohistochemistry | Rabbits | Cell Proliferation | Enzyme-Linked Immunosorbent Assay | Signal Transduction | Transforming Growth Factor beta1 - metabolism | Gene Expression Regulation | Smad2 Protein - metabolism | Nucleus Pulposus - pathology | Smad3 Protein - metabolism | Platelet-Rich Plasma - metabolism | Blotting, Western | Intervertebral Disc Degeneration - metabolism | Collagen Type II - metabolism | Intervertebral Disc Degeneration - pathology | Magnetic Resonance Imaging | Animals | Platelet Count | Real-Time Polymerase Chain Reaction | Intervertebral disc degeneration | Rabbit | Nucleus pulpous | Platelet-rich plasma | Cell proliferation | Collagen (type II) | Transforming growth factor | Collagens | mRNA | Nucleus pulposus | Intervertebral discs | Kinases | Recovery | Western blotting | Signal transduction | Blood platelets | Collagen (type X) | Smad2 protein | Extracellular matrix | Degeneration | Inhibition | Matrix protein | Growth factors | Wound healing | Tissue engineering | Injection | Gene expression | Magnetic resonance imaging | Collagen | Nuclei (cytology) | Aggrecan | Laboratory animals | Platelets | Binding sites | Smad2 | TGF‐β1 | Original
Journal Article
Brain Pathology, ISSN 1015-6305, 07/2018, Volume 28, Issue 4, pp. 495 - 506
Hereditary cerebral hemorrhage with amyloidosis‐Dutch type (HCHWA‐D) is an early onset hereditary form of cerebral amyloid angiopathy (CAA) pathology, caused... 
TGFβ | amyloid β mutation E22Q | postmortem human brain tissue | cerebral amyloid angiopathy | phospho‐SMAD2/3 granules | hereditary cerebral hemorrhage with amyloidosis‐Dutch type | hereditary cerebral hemorrhage with amyloidosis-Dutch type | phospho-SMAD2/3 granules | phospho-SMAD2 | SMALL VESSEL DISEASE | PROTEIN | ALZHEIMERS-DISEASE | PATHOLOGY | NEUROSCIENCES | COLOCALIZES | CLINICAL NEUROLOGY | amyloid beta mutation E22Q | 3 granules | MICROVASCULAR DEGENERATION | TRANSFORMING GROWTH-FACTOR-BETA-1 | ANGIOPATHY | TGF beta | EXPRESSION | TRANSGENIC MICE | TGF-BETA-1 | Up-Regulation | Phosphorylation | Frontal Lobe - metabolism | Signal Transduction | Humans | Middle Aged | Smad2 Protein - metabolism | Cerebral Amyloid Angiopathy, Familial - metabolism | Cerebral Amyloid Angiopathy, Familial - pathology | Male | Smad3 Protein - metabolism | Occipital Lobe - pathology | Occipital Lobe - blood supply | Aged, 80 and over | Female | Aged | Frontal Lobe - blood supply | Transforming Growth Factor beta - metabolism | Frontal Lobe - pathology | Occipital Lobe - metabolism | Immunohistochemistry | Brain | Deregulation | Pathogenesis | Transforming growth factor-a | Transgenic mice | Blood vessels | Gene expression | Hemorrhage | Lobes | Pathology | Cerebral amyloid angiopathy | Autopsy | Smad2 protein | Fibrosis | Biomarkers | β-Amyloid | Amyloidosis | Microvasculature | Occipital lobes
Journal Article
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
Journal Article
Journal of Cell Science, ISSN 0021-9533, 09/2017, Volume 130, Issue 18, pp. e1802 - e1802
Journal Article
Journal of Cellular Biochemistry, ISSN 0730-2312, 01/2019, Volume 120, Issue 1, pp. 93 - 104
Fibroblast‐to‐myofibroblast differentiation, which is characterized by increased expression of α‐smooth muscle actin, is known to be involved in the... 
transforming growth factor‐β1 (TGF‐β1)/Smad2 | fibroblast‐to‐myofibroblast differentiation | idiopathic pulmonary fibrosis | nuclear factor‐κB (NF‐κB) | sirtuin 6 (SIRT6) | fibroblast-to-myofibroblast differentiation | transforming growth factor-β1 (TGF-β1)/Smad2 | nuclear factor-κB (NF-κB) | Phosphorylation | Humans | Transforming Growth Factor beta1 - metabolism | Interleukin-1beta - genetics | NF-kappa B p50 Subunit - genetics | Lung - cytology | Idiopathic Pulmonary Fibrosis - metabolism | Myofibroblasts - metabolism | Transfection | Matrix Metalloproteinase 9 - genetics | Transcription, Genetic | Cell Differentiation | Sirtuins - genetics | Transforming Growth Factor beta1 - pharmacology | Cell Line | Cell Survival - drug effects | Lung - pathology | Interleukin-6 - genetics | NF-kappa B p50 Subunit - metabolism | Gene Expression Regulation | Smad2 Protein - metabolism | Reverse Transcriptase Polymerase Chain Reaction | Idiopathic Pulmonary Fibrosis - pathology | Cell Proliferation - drug effects | Sirtuins - metabolism | Histone deacetylase | Transcription | Mesenchyme | Pathogenesis | Transforming growth factor | Interleukin | Smooth muscle | Matrix metalloproteinase | Proteins | Signal transduction | Pathways | Actin | Smad2 protein | Fibroblasts | Metalloproteinase | Growth factors | Translocation | Fetuses | Lung diseases | Muscles | Gene expression | Nuclear transport | Signaling | Pulmonary fibrosis | Fibrosis | Differentiation
Journal Article