The study aims to elucidate how smoothened signaling affects myofibroblast activation and kidney fibrosis.
Characterization of smoothened signaling pathways in fibroblasts
Assessment of autophagy levels
Analysis of myofibroblast activation markers
In vitro modeling of kidney fibrosis
Increased smoothened signaling correlates with reduced autophagy in fibroblasts
Enhanced myofibroblast activation observed with smoothened activation
Potential target of fibroblast Smo identified for chronic kidney disease treatment
Abstract
Our study defines a prominent mechanism of myofibroblast activation and supplies a potential avenue for targeting fibroblast Smo to treat chronic kidney disease.