RNA Details
                    Disease Name
                    
                    idiopathic pulmonary fibrosis
                    
                    Tissue
                    
                    lung
                    
                    RNA Symbol
                    
                    SRF
                    
                RNA ID
                    
                    
                    
                RNA Type
                    
                    mRNA
                    
                Alteration Pattern
                    
                    up regulation
                    
                Species
                    
                    homo sapiens
                    
                Detection Methods
                    
                    Data compilation; Statistical analysis etc.
                    
                Target
                    
                    NA
                    
                Pathway
                    
                    NA
                    
                PubMed ID
                    
                    
                    
                    
                    
                Title
                    
                    Transcriptome of Cultured Lung Fibroblasts in Idiopathic Pulmonary Fibrosis: Meta-Analysis of Publically Available Microarray Datasets Reveals Repression of Inflammation and Immunity Pathways
                    
                Year
                    
                     2016
                    
                Function
                    
                    "SRF is a transcription factor that is activated by the p38 MAP kinase pathway [24] and by increased extracellular matrix stiffness through mechanotransduction [25]. SRF is essential for collagen-1 expression by lung fibroblasts in vitro [26], while inhibition of the SRF pathway by the small molecule CCG-203971 attenuates lung fibrogenesis in the bleomycin-induced lung fibrosis model in mice [27]. Interestingly, SRF drives CTGF expression in fibroblasts [28], raising the hypothesis that the stable overexpression of the SRF/CTGF axis may contribute to the heritable profibrotic phenotype of lung fibroblasts in IPF."