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Chromomycin A3 inhibits DNA replication and transcription, blocks the binding of Sp1 transcription factor to target gene promoters, downregulates the expression of anti-apoptotic proteins such as FLIP, Mcl-1, and XIAP, and induces S-phase cycle arrest and caspase-dependent apoptosis in tumor cells

including the protective role of some antioxidants

We explore the evidence for alveolar epithelial cell (AEC) apoptosis being important in promoting asbestosis and IPF with an emphasis on ROS derived from the mitochondria- and p53-regulated death pathways as well as recent evidence for an activated endoplasmic reticulum (ER) stress response in patients with IPF

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