Perk is dispensable for smooth muscle cell phenotype switching in atherosclerosis

Unfolded protein response (UPR) markers, thin fibrous caps, and inflammation correlate with human lesion instability and rupture. In mice, UPR drives macrophage and endothelial apoptosis and inflammation, but its impact on lesion stability through SMC modulation is debated.

The UPR protein Perk was recently shown to drive SMC modulation in vivo, suggesting that depletion of SMC Perk may regulate lesion stability. We sought to determine if inducible SMC-specific Perk deletion in adult mice improves characterizations of lesion stability during development and progression of disease.