COL1A1 and idiopathic pulmonary fibrosis: Therefore, in all, mechanosensory studies corroborate the findings that exposure of fibroblasts to a microenvironment mimicking increased pathological stiffnesses encountered in chronic lung diseases such as IPF and COPD activates and increases the expression of mechanotransduction transcription factors (YAP, TAZ), fibrotic genes (ACTA2, COL-1A1, FBLN1) and proteins that contribute to pathological mechanisms in chronic lung disease.