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\ No newline at end of file

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\ No newline at end of file

+Diagnostic Values For Club Cell Secretory Protein (CC16) in Serum of Patients of Combined Pulmonary Fibrosis and Emphysema
+Epigenetic Regulation of Caveolin-1 Gene Expression in Lung Fibroblasts
+Targeting of Discoidin Domain Receptor 2 (DDR2) Prevents Myofibroblast Activation and Neovessel Formation During Pulmonary Fibrosis
+Epithelial Cell Mitochondrial Dysfunction and PINK1 Are Induced by Transforming Growth Factor- Beta1 in Pulmonary Fibrosis
+The lncRNA H19 Mediates Pulmonary Fibrosis by Regulating the miR-196a/COL1A1 Axis
+Inhibition of PHGDH Attenuates Bleomycin-induced Pulmonary Fibrosis
+Transforming Growth Factor Beta 1 Activation, Storage, and Signaling Pathways in Idiopathic Pulmonary Fibrosis in Dogs
+Developmental Reprogramming in Mesenchymal Stromal Cells of Human Subjects with Idiopathic Pulmonary Fibrosis
+Autoimmunity to Vimentin Is Associated with Outcomes of Patients with Idiopathic Pulmonary Fibrosis
+Amplification of TGFb Induced ITGB6 Gene Transcription May Promote Pulmonary Fibrosis
+Macrophage Bone Morphogenic Protein Receptor 2 (BMPR2) depletion in Idiopathic Pulmonary Fibrosis (IPF) and Group III Pulmonary Hypertension
+Resveratrol-Mediated Repression and Reversion of Prostatic Myofibroblast Phenoconversion
+Sunitinib, a Small-Molecule Kinase Inhibitor, Attenuates Bleomycin-Induced Pulmonary Fibrosis in Mice
+Differing Expression of Cytokines and Tumor Markers in Combined Pulmonary Fibrosis and Emphysema Compared to Emphysema and Pulmonary Fibrosis
+miR-18a-5p Inhibits Sub-pleural Pulmonary Fibrosis by Targeting TGF-b Receptor II
+Hyper-responsiveness of IPF/UIP fibroblasts: interplay between TGFbeta1, IL-13 and CCL2
+Protective Effect of Ginsenoside Rg1 on Bleomycin-Induced Pulmonary Fibrosis in Rats: Involvement of Caveolin-1 and TGF-b1 Signal Pathway
+Mesenchymal Stem Cells Correct Inappropriate Epithelial-mesenchyme Relation in Pulmonary Fibrosis Using Stanniocalcin-1
+Chop Deficiency Protects Mice Against Bleomycin-induced Pulmonary Fibrosis by Attenuating M2 Macrophage Production
+Transforming Growth Factor (TGF)-b Promotes de Novo Serine Synthesis for Collagen Production
+Two-Way Conversion between Lipogenic and Myogenic Fibroblastic Phenotypes Marks the Progression and Resolution of Lung Fibrosis
+Normal Human Lung Epithelial Cells Inhibit Transforming Growth Factor-b Induced Myofibroblast Differentiation via Prostaglandin E2
+Inhibition of the KCa3.1 Channel Alleviates Established Pulmonary Fibrosis in a Large Animal Model
+AKT2 Regulates Pulmonary Inflammation and Fibrosis via Modulating Macrophage Activation
+Novel Mechanisms for the Antifibrotic Action of Nintedanib
+Determining the True Selectivity Profile of av Integrin Ligands Using Radioligand Binding: Applying an Old Solution to a New Problem
+Increased Galectin-9 Concentration and Number of CD4+Foxp3high+Cells in Bronchoalveolar Lavage Fluid of Patients with Cryptogenic Organizing Pneumonia
+Reduced Ets Domain-containing Protein Elk1 Promotes Pulmonary Fibrosis via Increased Integrin avb6 Expression
+Expression of RXFP1 Is Decreased in Idiopathic Pulmonary Fibrosis
+The Anti-fibrotic Effects and Mechanisms of MicroRNA-486-5p in Pulmonary Fibrosis
+MAP3K19 Is a Novel Regulator of TGF-b Signaling That Impacts Bleomycin-Induced Lung Injury and Pulmonary Fibrosis
+Dysregulated Collagen Homeostasis by Matrix Stiffening and TGF-b1 in Fibroblasts from Idiopathic Pulmonary Fibrosis Patients: Role of FAK/Akt
+Sustained Activation of Toll-Like Receptor 9 Induces an Invasive Phenotype in Lung Fibroblasts: Possible Implications in Idiopathic Pulmonary Fibrosis
+Regulation of 26S Proteasome Activity in Pulmonary Fibrosis
+Membrane-anchored Serine Protease Matriptase Is a Trigger of Pulmonary Fibrogenesis
+The Role of PPARs in Lung Fibrosis
+Lipoxin A4 Attenuates Constitutive and TGF-b1-Dependent Profibrotic Activity in Human Lung Myofibroblasts
+Cigarette Smoke Enhances the Expression of Profibrotic Molecules in Alveolar Epithelial Cells
+Idiopathic Pulmonary Fibrosis: Aging, Mitochondrial Dysfunction, and Cellular Bioenergetics
+CXCL9 Regulates TGF-b1-Induced Epithelial to Mesenchymal Transition in Human Alveolar Epithelial Cells
+Anti-fibrotic Role of aB-crystallin Inhibition in Pleural and Subpleural Fibrosis
+Expression of WNT5A in Idiopathic Pulmonary Fibrosis and Its Control by TGF-b and WNT7B in Human Lung Fibroblasts

+<r>Regulation </r>of human lung fibroblast <g>C1q</g>-receptors by <g>transforming growth factor-beta</g> and <g>tumor necrosis factor-alpha</g>
+High levels of <g>IL-6</g> and <g>IL-8</g> characterize early-on <d>idiopathic pulmonary fibrosis</d> acute exacerbations
+Regulation of the effects of <g>TGF-beta 1</g> by activation of latent <g>TGF-beta 1</g> and differential <e>expression </e>of <g>TGF-beta receptors (T beta R-I and T beta R-II</g>) in <d>idiopathic pulmonary fibrosis</d>
+Peripheral depletion of NK cells and imbalance of the Treg/Th17 axis in <d>idiopathic pulmonary fibrosis</d> patients
+<g>miR-9-5p</g> suppresses pro-fibrogenic transformation of fibroblasts and prevents organ <d>fibrosis</d> by targeting <g>NOX4</g> and <g>TGFBR2</g>
+Profibrotic role of <g>WNT10A</g> via <g>TGF-b</g> signaling in <d>idiopathic pulmonary fibrosis</d>
+Microarray profiling reveals <u>suppressed </u>interferon stimulated gene program in fibroblasts from scleroderma-associated <d>interstitial lung disease</d>
+<g>IL-4</g> polymorphisms, HRCT score and lung tissue markers in <d>idiopathic pulmonary fibrosis</d>
+Herpes <d>virus infection</d> is associated with vascular remodeling and <d>pulmonary hypertension</d> in <d>idiopathic pulmonary fibrosis</d>
+Microencapsulation of lefty-secreting engineered cells for <d>pulmonary fibrosis</d> therapy in mice
+Targeting of <g>Discoidin Domain Receptor 2</g> (<g>DDR2</g>) Prevents Myofibroblast Activation and Neovessel Formation During <d>Pulmonary Fibrosis</d>
+Role of <g>protease-activated receptor-2</g> in <d>idiopathic pulmonary fibrosis</d>
+<g>Chop</g>
+<g>VCAM-1</g> is a <g>TGF-b1</g> inducible gene <v>upregulated </v>in <d>idiopathic pulmonary fibrosis</d>
+<u>Suppression </u>of <g>plasminogen activator inhibitor-1</g> by RNA interference attenuates <d>pulmonary fibrosis</d>
+<g>JAK2</g> mediates <d>lung fibrosis</d>, <d>pulmonary vascular remodelling</d> and <d>hypertension</d> in <d>idiopathic pulmonary fibrosis</d>: an experimental study
+Melatonin attenuates <g>TGFb1</g>-induced epithelial-mesenchymal transition in lung alveolar epithelial cells
+<r>Deregulation </r>of selective autophagy during aging and <d>pulmonary fibrosis</d>: the role of <g>TGFb1</g>
+<g>RhoA</g> signaling <r>modulates </r><g>cyclin D1</g> <e>expression </e>in human lung fibroblasts; implications for <d>idiopathic pulmonary fibrosis</d>
+Inhibitory effect of <g>receptor for advanced glycation end products</g> (<g>RAGE</g>) on the <g>TGF-b</g>-induced alveolar epithelial to mesenchymal transition
+<e>Effects </e>of the <d>tumor</d> suppressor <g>PTEN</g> on the pathogenesis of <d>idiopathic pulmonary fibrosis</d> in Chinese patients
+Triptolide suppresses paraquat induced <d>idiopathic pulmonary fibrosis</d> by inhibiting <g>TGFB1</g>-dependent epithelial mesenchymal transition
+<g>Endothelin-1</g> <v>induces </v>alveolar epithelial-mesenchymal transition through endothelin type A receptor-<v>mediated </v><e>production </e>of <g>TGF-beta1</g>
+<g>p63</g> - Key molecule in the early phase of <d>epithelial abnormality</d> in <d>idiopathic pulmonary fibrosis</d>
+The hedgehog system machinery controls transforming growth factor-b-dependent myofibroblastic differentiation in humans: involvement in <d>idiopathic pulmonary fibrosis</d>
+<v>Upregulation </v>of <g>activin</g>-B and <g>follistatin</g> in <d>pulmonary fibrosis</d> - a translational study using human biopsies and a specific inhibitor in mouse <d>fibrosis</d> models
+<u>Inhibition </u>of the <g>KCa3.1</g>
+Current and novel drug therapies for <d>idiopathic pulmonary fibrosis</d>
+<g>Protease activated receptor-1</g> regulates macrophage-mediated cellular senescence: a risk for <d>idiopathic pulmonary fibrosis</d>
+Sphingolipids in <d>pulmonary fibrosis</d>
+Sirtuin 7 is decreased in pulmonary fibrosis and regulates the fibrotic phenotype of lung fibroblasts
+Pirfenidone for the treatment of <d>idiopathic pulmonary fibrosis</d>
+The anti-fibrotic effect of <u>inhibition </u>of <g>TGFb</g>-<g>ALK5</g> signalling in experimental <d>pulmonary fibrosis</d> in mice is attenuated in the presence of concurrent y-herpesvirus infection
+Angiotensin-<g>TGF-beta</g> 1 crosstalk in human <d>idiopathic pulmonary fibrosis</d>: autocrine mechanisms in myofibroblasts and macrophages
+SNAI transcription factors mediate epithelial-mesenchymal transition in <d>lung fibrosis</d>
+<g>MiR-338</g>* suppresses fibrotic pathogenesis in <d>pulmonary fibrosis</d> through targeting <g>LPA1</g>
+BALF N-acetylglucosaminidase and <g>beta-galactosidase</g> activities in <d>idiopathic pulmonary fibrosis</d>
+<g>Th1</g>/Th2 cytokine gene polymorphisms in patients with <d>idiopathic pulmonary fibrosis</d>
+Transforming Growth Factor (TGF)-b Promotes de Novo Serine Synthesis for Collagen <e>Production.</e> <g>TGF-b</g> <v>promotes </v>excessive collagen deposition in <d>fibrotic diseases</d> such as <d>idiopathic pulmonary fibrosis</d> (<d>IPF</d>)
+The Epstein-Barr virus latent membrane protein 1 and transforming growth factor--b1 synergistically induce epithelial--mesenchymal transition in lung epithelial cells
+<g>Transcription factor GATA-6</g> is <e>expressed </e>in quiescent myofibroblasts in <d>idiopathic pulmonary fibrosis</d>
+Epithelial-to-mesenchymal transition and its role in <g>EGFR</g>-mutant <d>lung adenocarcinoma</d> and <d>idiopathic pulmonary fibrosis</d>

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+Tissue inhibitor of metalloproteinase-3 is up-regulated by transforming growth factor-beta1 in vitro and expressed in fibroblastic foci in vivo in idiopathic pulmonary fibrosis
+Upregulation of alveolar levels of activin B, but not activin A, in lungs of west highland white terriers with idiopathic pulmonary fibrosis and diffuse alveolar damage
+Progressive transforming growth factor beta1-induced lung fibrosis is blocked by an orally active ALK5 kinase inhibitor
+Upregulation of activin-B and follistatin in pulmonary fibrosis - a translational study using human biopsies and a specific inhibitor in mouse fibrosis models
+Resveratrol inhibits transforming growth factor-b-induced proliferation and differentiation of ex vivo human lung fibroblasts into myofibroblasts through ERK/Akt inhibition and PTEN restoration
+Interactions between b-catenin and transforming growth factor-b signaling pathways mediate epithelial-mesenchymal transition and are dependent on the transcriptional co-activator cAMP-response element-binding protein (CREB)-binding protein (CBP)
+Syndecan-2 exerts antifibrotic effects by promoting caveolin-1-mediated transforming growth factor-b receptor I internalization and inhibiting transforming growth factor-b1 signaling
+Lower expression of platelet derived growth factor is associated with better overall survival rate of patients with idiopathic nonspecific interstitial pneumonia
+TGF-beta 1, but not TGF-beta 2 or TGF-beta 3, is differentially present in epithelial cells of advanced pulmonary fibrosis: an immunohistochemical study
+Induction of epithelial-mesenchymal transition in alveolar epithelial cells by transforming growth factor-beta1: potential role in idiopathic pulmonary fibrosis
+Significance of elevated procollagen-III-peptide and transforming growth factor-beta levels of bronchoalveolar lavage fluids from idiopathic pulmonary fibrosis patients
+The latent form of TGFbeta(1) is induced by TNFalpha through an ERK specific pathway and is activated by asbestos-derived reactive oxygen species in vitro and in vivo
+Human placental mesenchymal stem cells of fetal origins-alleviated inflammation and fibrosis by attenuating MyD88 signaling in bleomycin-induced pulmonary fibrosis mice
+Fibroblasts from idiopathic pulmonary fibrosis and normal lungs differ in growth rate, apoptosis, and tissue inhibitor of metalloproteinases expression
+Phosphatase and tensin homolog deleted on chromosome 10 contributes to phenotype transformation of fibroblasts in idiopathic pulmonary fibrosis via multiple pathways
+Transforming growth factor-b1 downregulates vascular endothelial growth factor-D expression in human lung fibroblasts via the Jun NH2-terminal kinase signaling pathway
+The anti-fibrotic effect of inhibition of TGFb-ALK5 signalling in experimental pulmonary fibrosis in mice is attenuated in the presence of concurrent y-herpesvirus infection
+Transforming growth factor-b inhibits IQ motif containing guanosine triphosphatase activating protein  1 expression in lung fibroblasts via the nuclear factor-kB signaling pathway
+De-ubiquitinating enzyme, USP11, promotes transforming growth factor b-1 signaling through stabilization of transforming growth factor b receptor II
+Aortic carboxypeptidase-like protein (ACLP) enhances lung myofibroblast differentiation through transforming growth factor b receptor-dependent and -independent pathways
+Insulin-like growth factor binding proteins 3 and 5 are overexpressed in idiopathic pulmonary fibrosis and contribute to extracellular matrix deposition
+Bile acids induce activation of alveolar epithelial cells and lung fibroblasts through farnesoid X receptor-dependent and independent pathways
+Fibroblastic foci, covered with alveolar epithelia exhibiting epithelial-mesenchymal transition, destroy alveolar septa by disrupting blood flow in idiopathic pulmonary fibrosis
+Connective tissue growth factor expression and induction by transforming growth factor-beta is abrogated by simvastatin via a Rho signaling mechanism
+Sorafenib ameliorates bleomycin-induced pulmonary fibrosis: potential roles in the inhibition of epithelial-mesenchymal transition and fibroblast activation
+NOX4/NADPH oxidase expression is increased in pulmonary fibroblasts from patients with idiopathic pulmonary fibrosis and mediates TGFbeta1-induced fibroblast differentiation into myofibroblasts
+Idiopathic pulmonary fibrosis in relation to gene polymorphisms of transforming growth factor-b1 and plasminogen activator inhibitor 1
+Comparative study of transforming growth factor-b signalling and regulatory molecules in human and canine idiopathic pulmonary fibrosis
+Microsatellite instability in transforming growth factor-beta 1 type II receptor gene in alveolar lining epithelial cells of idiopathic pulmonary fibrosis
+Prostaglandin F(2alpha) receptor signaling facilitates bleomycin-induced pulmonary fibrosis independently of transforming growth factor-beta
+Sphingosine-1-phosphate is increased in patients with idiopathic pulmonary fibrosis and mediates epithelial to mesenchymal transition
+Evaluation of permeability alteration and epithelial-mesenchymal transition induced by transforming growth factor-b1 in A549, NCI-H441, and Calu-3 cells: Development of an in vitro model of respiratory epithelial cells in idiopathic pulmonary fibrosis
+TGF-b1 stimulates HDAC4 nucleus-to-cytoplasm translocation and NADPH oxidase 4-derived reactive oxygen species in normal human lung fibroblasts
+Lactic acid is elevated in idiopathic pulmonary fibrosis and induces myofibroblast differentiation via pH-dependent activation of transforming growth factor-b
+Differential mRNA expression of insulin-like growth factor-1 splice variants in patients with idiopathic pulmonary fibrosis and pulmonary sarcoidosis
+The hedgehog system machinery controls transforming growth factor-b-dependent myofibroblastic differentiation in humans: involvement in idiopathic pulmonary fibrosis
+Reactive oxygen species are required for maintenance and differentiation of primary lung fibroblasts in idiopathic pulmonary fibrosis
+Are mast cells instrumental for fibrotic diseases? Idiopathic pulmonary fibrosis (IPF) is a fatal lung disorder of unknown etiology characterized by accumulation of lung fibroblasts and extracellular matrix deposition, ultimately leading to compromised tissue architecture and lung function capacity
+The role of halofuginone in fibrosis: more to be explored? Fibrosis, which can be defined as an abnormal or excessive accumulation of extracellular matrix (ECM), particularly fibrillar collagens, is a key driver of progressive organ dysfunction in many inflammatory and metabolic diseases, including idiopathic pulmonary fibrosis (IPF), cirrhosis, nephropathy, and oral submucous fibrosis (OSF)
+CCN5 overexpression inhibits profibrotic phenotypes via the PI3K/Akt signaling pathway in lung fibroblasts isolated from patients with idiopathic pulmonary fibrosis and in an in vivo model of lung fibrosis
+Mast cell chymase: an indispensable instrument in the pathological symphony of idiopathic pulmonary fibrosis? Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive and fatal lung disease with no known etiology and treatment options
+The Epstein-Barr virus latent membrane protein 1 and transforming growth factor--b1 synergistically induce epithelial--mesenchymal transition in lung epithelial cells
+PI3K p110y overexpression in idiopathic pulmonary fibrosis lung tissue and fibroblast cells: in vitro effects of its inhibition
+Rapamycin regulates connective tissue growth factor expression of lung epithelial cells via phosphoinositide 3-kinase
+Proliferation of pulmonary interstitial fibroblasts is mediated by transforming growth factor-beta1-induced release of extracellular fibroblast growth factor-2 and phosphorylation of p38 MAPK and JNK
+Secreted protein acidic and rich in cysteine (SPARC) is upregulated by transforming growth factor (TGF)-b and is required for TGF-b-induced hydrogen peroxide production in fibroblasts
+Semaphorin 7a+ regulatory T cells are associated with progressive idiopathic pulmonary fibrosis and are implicated in transforming growth factor-b1-induced pulmonary fibrosis
+Arsenic trioxide inhibits transforming growth factor-b1-induced fibroblast to myofibroblast differentiation in vitro and bleomycin induced lung fibrosis in vivo

+Resveratrol inhibits transforming growth factor-b-induced proliferation and differentiation of ex vivo human lung fibroblasts into myofibroblasts through <g>ERK</g>/<g>Akt</g> <u>inhibition </u>and <g>PTEN</g> restoration
+Signaling pathways in the epithelial origins of <d>pulmonary fibrosis</d>
+Raised serum levels of <g>IGFBP-1</g> and <g>IGFBP-2</g> in <d>idiopathic pulmonary fibrosis</d>
+Methylation-mediated <g>BMPER</g> <e>expression </e>in fibroblast activation in vitro and lung <d>fibrosis</d> in mice in vivo
+<d>Fibrosis</d> of two: Epithelial cell-fibroblast interactions in <d>pulmonary fibrosis</d>
+Arsenic trioxide inhibits transforming growth factor-b1-induced <d>fibroblast to myofibroblast differentiation</d> in vitro and bleomycin induced lung <d>fibrosis</d> in vivo
+microRNA-1343 attenuates pathways of <d>fibrosis</d> by targeting the <g>TGF-b</g> receptors
+<g>Matrix metalloproteinase (MMP)-19</g> <u>deficient </u>fibroblasts display a profibrotic phenotype
+Comparative study of transforming growth factor-b signalling and regulatory molecules in human and canine <d>idiopathic pulmonary fibrosis</d>
+Genetic polymorphism in <g>matrix metalloproteinase-9</g> and <g>transforming growth factor-b1</g> and susceptibility to <d>combined pulmonary fibrosis</d> and <d>emphysema</d> in  a Chinese population
+Transforming growth factor-b1 downregulates <g>vascular endothelial growth factor</g>-D expression in human lung fibroblasts via the <g>Jun NH2-terminal kinase</g> signaling pathway
+<g>Ubiquitin carboxyl-terminal hydrolase-L5</g> promotes <g>TGFb-1</g> signaling by de-ubiquitinating and stabilizing <g>Smad2</g>/<g>Smad3</g> in <d>pulmonary fibrosis</d>
+Effect of pirfenidone on proliferation, <g>TGF-b</g>-induced myofibroblast differentiation and fibrogenic activity of primary human lung fibroblasts
+[Quantifying plasma levels of <g>transforming growth factor beta1</g> in <d>idiopathic pulmonary fibrosis</d>]
+The matricellular protein <g>CCN1</g> enhances <g>TGF-b1</g>/<g>SMAD3</g>-dependent profibrotic signaling in fibroblasts and contributes to fibrogenic responses to <d>lung injury</d>
+Bleomycin in the setting of <d>lung fibrosis</d> induction: From biological mechanisms to counteractions
+Alveolar epithelial cell injury with Epstein-Barr virus <v>upregulates </v><g>TGFbeta1</g> <e>expression.</e> <d>Idiopathic pulmonary fibrosis</d> (<d>IPF</d>) is a refractory and lethal <d>interstitial lung disease</d> characterized by alveolar epithelial cells apoptosis, fibroblast proliferation, and ECM protein deposition
+Single-cell RNA sequencing identifies diverse roles of epithelial cells in <d>idiopathic pulmonary fibrosis</d>
+Data on <g>CUX1</g> isoforms in <d>idiopathic pulmonary fibrosis lung</d> and <d>systemic sclerosis</d> skin tissue sections
+<d>Idiopathic Pulmonary Fibrosis</d>: Aging, Mitochondrial Dysfunction, and Cellular Bioenergetics
+Genetic partitioning of <g>interleukin-6</g> signalling in mice dissociates <g>Stat3</g> from <g>Smad3</g>-mediated <d>lung fibrosis</d>
+Reactive oxygen species are required for maintenance and differentiation of primary lung fibroblasts in <d>idiopathic pulmonary fibrosis</d>
+Oxidant-antioxidant imbalance as a potential contributor to the progression of human <d>pulmonary fibrosis</d>
+Increased production and immunohistochemical localization of <g>transforming growth factor-beta</g> in <d>idiopathic pulmonary fibrosis</d>
+Type V collagen induced tolerance suppresses collagen deposition, <g>TGF-b</g> and associated transcripts in <d>pulmonary fibrosis</d>
+Preventive and therapeutic effects of thymosin b4 N-terminal fragment Ac-SDKP in the bleomycin model of pulmonary fibrosis
+FAK-related nonkinase is a multifunctional negative regulator of <d>pulmonary fibrosis</d>
+Nitrated fatty acids reverse <d>pulmonary fibrosis</d> by dedifferentiating myofibroblasts and promoting collagen uptake by alveolar macrophages
+Cytokine profiles in <d>idiopathic pulmonary fibrosis</d> suggest an important role for <g>TGF-beta</g> and <g>IL-10</g>
+Sphingosine-1-phosphate is increased in patients with <d>idiopathic pulmonary fibrosis</d> and mediates epithelial to mesenchymal transition
+Leucine-rich a-2 glycoprotein promotes <d>lung fibrosis</d> by modulating <g>TGF-b</g> signaling in fibroblasts
+Sustained <g>PI3K</g>
+Pirfenidone <u>inhibits </u>the <e>expression </e>of <g>HSP47</g> in <g>TGF-beta1</g>-stimulated human lung fibroblasts
+Age-driven developmental drift in the pathogenesis of <d>idiopathic pulmonary fibrosis</d>
+Endogenous <g>Semaphorin-7A</g>
+Progressive transforming growth factor beta1-induced <d>lung fibrosis</d> is blocked by an orally active <g>ALK5</g> kinase <u>inhibitor.</u> <d>Pulmonary fibrosis</d> is characterized by chronic scar formation and deposition of extracellular matrix, resulting in <d>impaired lung function</d> and <d>respiratory failure</d>
+Compromised peroxisomes in <d>idiopathic pulmonary fibrosis</d>, a vicious cycle inducing a higher fibrotic response via <g>TGF-b</g> signaling
+Inhibition of NF-kappaB signaling reduces virus load and gammaherpesvirus-induced <d>pulmonary fibrosis</d>
+Intrinsic defence capacity and therapeutic potential of natriuretic peptides in <d>pulmonary hypertension</d> associated with <d>lung fibrosis</d>
+Possible involvement of pirfenidone metabolites in the antifibrotic action of a therapy for <d>idiopathic pulmonary fibrosis</d>
+BAL cytokine profile in different <d>interstitial lung diseases</d>: a focus on <d>systemic sclerosis</d>
+Matrix metalloproteinase 3 is a mediator of <d>pulmonary fibrosis</d>
+<u>Inhibition </u>of <g>PHGDH</g>
+Bleomycin induces molecular changes directly relevant to <d>idiopathic pulmonary fibrosis</d>: a model for "active" disease
+Lysyl oxidases <r>regulate </r>fibrillar collagen remodelling in idiopathic pulmonary fibrosis
+Discovery and validation of extracellular/circulating microRNAs during <d>idiopathic pulmonary fibrosis disease</d> progression
+Recombinant human <g>serum amyloid P</g> in healthy volunteers and patients with <d>pulmonary fibrosis</d>
+<g>Transforming Growth Factor Beta 1</g>

+Diagnostic Values For Club Cell Secretory Protein (CC16) in Serum of Patients of Combined Pulmonary Fibrosis and Emphysema
+Epigenetic Regulation of Caveolin-1 Gene Expression in Lung Fibroblasts
+Targeting of Discoidin Domain Receptor 2 (DDR2) Prevents Myofibroblast Activation and Neovessel Formation During Pulmonary Fibrosis
+Epithelial Cell Mitochondrial Dysfunction and PINK1 Are Induced by Transforming Growth Factor- Beta1 in Pulmonary Fibrosis
+The lncRNA H19 Mediates Pulmonary Fibrosis by Regulating the miR-196a/COL1A1 Axis
+Inhibition of PHGDH Attenuates Bleomycin-induced Pulmonary Fibrosis
+Transforming Growth Factor Beta 1 Activation, Storage, and Signaling Pathways in Idiopathic Pulmonary Fibrosis in Dogs
+Developmental Reprogramming in Mesenchymal Stromal Cells of Human Subjects with Idiopathic Pulmonary Fibrosis
+Autoimmunity to Vimentin Is Associated with Outcomes of Patients with Idiopathic Pulmonary Fibrosis
+Amplification of TGFb Induced ITGB6 Gene Transcription May Promote Pulmonary Fibrosis
+Macrophage Bone Morphogenic Protein Receptor 2 (BMPR2) depletion in Idiopathic Pulmonary Fibrosis (IPF) and Group III Pulmonary Hypertension
+Resveratrol-Mediated Repression and Reversion of Prostatic Myofibroblast Phenoconversion
+Sunitinib, a Small-Molecule Kinase Inhibitor, Attenuates Bleomycin-Induced Pulmonary Fibrosis in Mice
+Differing Expression of Cytokines and Tumor Markers in Combined Pulmonary Fibrosis and Emphysema Compared to Emphysema and Pulmonary Fibrosis
+miR-18a-5p Inhibits Sub-pleural Pulmonary Fibrosis by Targeting TGF-b Receptor II
+Hyper-responsiveness of IPF/UIP fibroblasts: interplay between TGFbeta1, IL-13 and CCL2
+Protective Effect of Ginsenoside Rg1 on Bleomycin-Induced Pulmonary Fibrosis in Rats: Involvement of Caveolin-1 and TGF-b1 Signal Pathway
+Mesenchymal Stem Cells Correct Inappropriate Epithelial-mesenchyme Relation in Pulmonary Fibrosis Using Stanniocalcin-1
+Chop Deficiency Protects Mice Against Bleomycin-induced Pulmonary Fibrosis by Attenuating M2 Macrophage Production
+Transforming Growth Factor (TGF)-b Promotes de Novo Serine Synthesis for Collagen Production
+Two-Way Conversion between Lipogenic and Myogenic Fibroblastic Phenotypes Marks the Progression and Resolution of Lung Fibrosis
+Normal Human Lung Epithelial Cells Inhibit Transforming Growth Factor-b Induced Myofibroblast Differentiation via Prostaglandin E2
+Inhibition of the KCa3.1 Channel Alleviates Established Pulmonary Fibrosis in a Large Animal Model
+AKT2 Regulates Pulmonary Inflammation and Fibrosis via Modulating Macrophage Activation
+Novel Mechanisms for the Antifibrotic Action of Nintedanib
+Determining the True Selectivity Profile of av Integrin Ligands Using Radioligand Binding: Applying an Old Solution to a New Problem
+Increased Galectin-9 Concentration and Number of CD4+Foxp3high+Cells in Bronchoalveolar Lavage Fluid of Patients with Cryptogenic Organizing Pneumonia
+Reduced Ets Domain-containing Protein Elk1 Promotes Pulmonary Fibrosis via Increased Integrin avb6 Expression
+Expression of RXFP1 Is Decreased in Idiopathic Pulmonary Fibrosis
+The Anti-fibrotic Effects and Mechanisms of MicroRNA-486-5p in Pulmonary Fibrosis
+MAP3K19 Is a Novel Regulator of TGF-b Signaling That Impacts Bleomycin-Induced Lung Injury and Pulmonary Fibrosis
+Dysregulated Collagen Homeostasis by Matrix Stiffening and TGF-b1 in Fibroblasts from Idiopathic Pulmonary Fibrosis Patients: Role of FAK/Akt
+Sustained Activation of Toll-Like Receptor 9 Induces an Invasive Phenotype in Lung Fibroblasts: Possible Implications in Idiopathic Pulmonary Fibrosis
+Regulation of 26S Proteasome Activity in Pulmonary Fibrosis
+Membrane-anchored Serine Protease Matriptase Is a Trigger of Pulmonary Fibrogenesis
+The Role of PPARs in Lung Fibrosis
+Lipoxin A4 Attenuates Constitutive and TGF-b1-Dependent Profibrotic Activity in Human Lung Myofibroblasts
+Cigarette Smoke Enhances the Expression of Profibrotic Molecules in Alveolar Epithelial Cells
+Idiopathic Pulmonary Fibrosis: Aging, Mitochondrial Dysfunction, and Cellular Bioenergetics
+CXCL9 Regulates TGF-b1-Induced Epithelial to Mesenchymal Transition in Human Alveolar Epithelial Cells
+Anti-fibrotic Role of aB-crystallin Inhibition in Pleural and Subpleural Fibrosis
+Expression of WNT5A in Idiopathic Pulmonary Fibrosis and Its Control by TGF-b and WNT7B in Human Lung Fibroblasts

+<r>Regulation </r>of human lung fibroblast <g>C1q</g>-receptors by <g>transforming growth factor-beta</g> and <g>tumor necrosis factor-alpha</g>
+High levels of <g>IL-6</g> and <g>IL-8</g> characterize early-on <d>idiopathic pulmonary fibrosis</d> acute exacerbations
+Regulation of the effects of <g>TGF-beta 1</g> by activation of latent <g>TGF-beta 1</g> and differential <e>expression </e>of <g>TGF-beta receptors (T beta R-I and T beta R-II</g>) in <d>idiopathic pulmonary fibrosis</d>
+Peripheral depletion of NK cells and imbalance of the Treg/Th17 axis in <d>idiopathic pulmonary fibrosis</d> patients
+<g>miR-9-5p</g> suppresses pro-fibrogenic transformation of fibroblasts and prevents organ <d>fibrosis</d> by targeting <g>NOX4</g> and <g>TGFBR2</g>
+Profibrotic role of <g>WNT10A</g> via <g>TGF-b</g> signaling in <d>idiopathic pulmonary fibrosis</d>
+Microarray profiling reveals <u>suppressed </u>interferon stimulated gene program in fibroblasts from scleroderma-associated <d>interstitial lung disease</d>
+<g>IL-4</g> polymorphisms, HRCT score and lung tissue markers in <d>idiopathic pulmonary fibrosis</d>
+Herpes <d>virus infection</d> is associated with vascular remodeling and <d>pulmonary hypertension</d> in <d>idiopathic pulmonary fibrosis</d>
+Microencapsulation of lefty-secreting engineered cells for <d>pulmonary fibrosis</d> therapy in mice
+Targeting of <g>Discoidin Domain Receptor 2</g> (<g>DDR2</g>) Prevents Myofibroblast Activation and Neovessel Formation During <d>Pulmonary Fibrosis</d>
+Role of <g>protease-activated receptor-2</g> in <d>idiopathic pulmonary fibrosis</d>
+<g>Chop</g>
+<g>VCAM-1</g> is a <g>TGF-b1</g> inducible gene <v>upregulated </v>in <d>idiopathic pulmonary fibrosis</d>
+<u>Suppression </u>of <g>plasminogen activator inhibitor-1</g> by RNA interference attenuates <d>pulmonary fibrosis</d>
+<g>JAK2</g> mediates <d>lung fibrosis</d>, <d>pulmonary vascular remodelling</d> and <d>hypertension</d> in <d>idiopathic pulmonary fibrosis</d>: an experimental study
+Melatonin attenuates <g>TGFb1</g>-induced epithelial-mesenchymal transition in lung alveolar epithelial cells
+<r>Deregulation </r>of selective autophagy during aging and <d>pulmonary fibrosis</d>: the role of <g>TGFb1</g>
+<g>RhoA</g> signaling <r>modulates </r><g>cyclin D1</g> <e>expression </e>in human lung fibroblasts; implications for <d>idiopathic pulmonary fibrosis</d>
+Inhibitory effect of <g>receptor for advanced glycation end products</g> (<g>RAGE</g>) on the <g>TGF-b</g>-induced alveolar epithelial to mesenchymal transition
+<e>Effects </e>of the <d>tumor</d> suppressor <g>PTEN</g> on the pathogenesis of <d>idiopathic pulmonary fibrosis</d> in Chinese patients
+Triptolide suppresses paraquat induced <d>idiopathic pulmonary fibrosis</d> by inhibiting <g>TGFB1</g>-dependent epithelial mesenchymal transition
+<g>Endothelin-1</g> <v>induces </v>alveolar epithelial-mesenchymal transition through endothelin type A receptor-<v>mediated </v><e>production </e>of <g>TGF-beta1</g>
+<g>p63</g> - Key molecule in the early phase of <d>epithelial abnormality</d> in <d>idiopathic pulmonary fibrosis</d>
+The hedgehog system machinery controls transforming growth factor-b-dependent myofibroblastic differentiation in humans: involvement in <d>idiopathic pulmonary fibrosis</d>
+<v>Upregulation </v>of <g>activin</g>-B and <g>follistatin</g> in <d>pulmonary fibrosis</d> - a translational study using human biopsies and a specific inhibitor in mouse <d>fibrosis</d> models
+<u>Inhibition </u>of the <g>KCa3.1</g>
+Current and novel drug therapies for <d>idiopathic pulmonary fibrosis</d>
+<g>Protease activated receptor-1</g> regulates macrophage-mediated cellular senescence: a risk for <d>idiopathic pulmonary fibrosis</d>
+Sphingolipids in <d>pulmonary fibrosis</d>
+Sirtuin 7 is decreased in pulmonary fibrosis and regulates the fibrotic phenotype of lung fibroblasts
+Pirfenidone for the treatment of <d>idiopathic pulmonary fibrosis</d>
+The anti-fibrotic effect of <u>inhibition </u>of <g>TGFb</g>-<g>ALK5</g> signalling in experimental <d>pulmonary fibrosis</d> in mice is attenuated in the presence of concurrent y-herpesvirus infection
+Angiotensin-<g>TGF-beta</g> 1 crosstalk in human <d>idiopathic pulmonary fibrosis</d>: autocrine mechanisms in myofibroblasts and macrophages
+SNAI transcription factors mediate epithelial-mesenchymal transition in <d>lung fibrosis</d>
+<g>MiR-338</g>* suppresses fibrotic pathogenesis in <d>pulmonary fibrosis</d> through targeting <g>LPA1</g>
+BALF N-acetylglucosaminidase and <g>beta-galactosidase</g> activities in <d>idiopathic pulmonary fibrosis</d>
+<g>Th1</g>/Th2 cytokine gene polymorphisms in patients with <d>idiopathic pulmonary fibrosis</d>
+Transforming Growth Factor (TGF)-b Promotes de Novo Serine Synthesis for Collagen <e>Production.</e> <g>TGF-b</g> <v>promotes </v>excessive collagen deposition in <d>fibrotic diseases</d> such as <d>idiopathic pulmonary fibrosis</d> (<d>IPF</d>)
+The Epstein-Barr virus latent membrane protein 1 and transforming growth factor--b1 synergistically induce epithelial--mesenchymal transition in lung epithelial cells
+<g>Transcription factor GATA-6</g> is <e>expressed </e>in quiescent myofibroblasts in <d>idiopathic pulmonary fibrosis</d>
+Epithelial-to-mesenchymal transition and its role in <g>EGFR</g>-mutant <d>lung adenocarcinoma</d> and <d>idiopathic pulmonary fibrosis</d>