PARP1 and idiopathic pulmonary fibrosis: Again, an obvious observation was, that pirfenidone-treatment was not associated with an induction of pro-apoptotic signaling, as compared to vehicle, whereas such was easily observed in response to LBH589-treatment of IPF-fibroblasts, as evident by the induction of the ER stress-factor CHOP (Fig 8D), the CHOP-target gene DR5 [55] (Fig 8E) and the mitochondrial apoptosis-inducing factor (AIF) (Fig 8F), which was paralleled by p53 (Fig 8G) and p21 upregulation (Fig 8H) as well as enhanced caspase-3- (Fig 8I) and PARP1-cleavage (Fig 8J).