Targeted suppression of CCR7/NF-κB signaling by apoptotic body-inspired colchicine nanovesicles halts atherosclerotic progression.

ABSTRACT: Atherosclerosis (AS) is a chronic inflammatory disorder characterized by foam cell formation and persistent inflammation as central pathological drivers. Although colchicine (Col) exhibits potent anti-inflammatory activities, its clinical application is limited by a narrow therapeutic window. In the present study, we developed phosphatidylserine-exposing nanovesicles (Col@PSVs) that leverage the innate phagocytic capacity of macrophage-derived foam cells by presenting surface "eat-me" signals, thereby enabling targeted immune modulation. The synergistic collaboration between Col and PSVs allows low-dose Col to retain robust anti-inflammatory efficacy while mitigating dose-dependent toxicity. Mechanistically, Col@PSVs potently suppress CCR7-mediated NF-κB signaling activation in foam cells,

SUBMITTER: Chen Q 

PROVIDER: S-EPMC12751986 | biostudies-literature | 2025 Nov

REPOSITORIES: biostudies-literature