TLR3 deficiency protects against collagen degradation and medial destruction in murine atherosclerotic plaques

Objective Inflammatory cell activation plays a key role in atherosclerotic plaque growth and acute complications. While secretion of proteases and inflammatory cytokines are likely involved in the development of plaque instability, the precise mechanistic pathways are not well understood. Methods and results Based on our previous study, we crossed Toll-like receptor 3 (Tlr3)−/− mice with a unique BALB-Apoe−/−Npc1−/− plaque...