Fig. 8: Schematic of the proposed model for the FBXL8-mediated proteasome degradation of Snail1 in cardiac fibrosis.

FBXL8 interacts with Snail1 and targets Snail1 for ubiquitin-proteasome degradation response to MI. In response to TGFβ stimulation and MI, downregulation of FBXL8 expression in CFs leads to stabilization of Snail1, thereby activating the RhoA/α-SMA pathway, inducing myofibroblast differentiation and the progress of cardiac fibrosis following MI.