Abstract
Fibrosis can be considered as wound healing that never ceases, and activated fibroblasts (myofibroblasts) probably play a critical role in this unabated tissue repair process. In the setting of renal fibrosis, two central questions remain unanswered: Where do activated myofibroblasts come from; and what mechanism or mechanisms keep them activated? The study by Chen and colleagues addresses the role of platelet-derived growth factor receptor (PDGFR) signaling in the activation of myofibroblasts.