Genomic Instability in Systemic Sclerosis is Promoted by a PERK/FOXO1-Dependent Axis
This study highlights a novel mechanism whereby genotoxic signals in dcSSc promote cell survival via a PERK/FOXO1-dependent axis and associated metabolic remodeling and provides mechanistic insights related to how changes to the mutational landscape reduce pro-fibrotic signals in DF after ASCT.