Complement Inhibition Targeted to Injury Specific Neoepitopes Attenuates Atherogenesis in Mice.

ABSTRACT: Rationale: Previous studies have indicated an important role for complement in atherosclerosis, a lipid-driven chronic inflammatory disease associated to oxidative stress in the vessel wall. However, it remains unclear how complement is activated in the process of atherogenesis. An accepted general model for complement activation in the context of ischemia reperfusion injury is that ischemia induces the exposure of neoepitopes that are recognized by natural self-reactive IgM antibodies, and that in turn activate complement. Objective: We investigated whether a similar phenomenon may be involved in the pathogenesis of atherosclerosis, and whether interfering with this activation event, together with inhibition of subsequent amplification of the cascade at the C3 activation ste

SUBMITTER: Dai S 

PROVIDER: S-EPMC8505745 | biostudies-literature | 2021

REPOSITORIES: biostudies-literature