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<p>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, leading to a marked downregulation of pro-inflammatory cytokine and disruption of inflammatory cascades. In <i>ApoE</i><sup><i>−/−</i></sup> AS mouse models, Col@PSVs treatment significantly improved plaque stability and attenuated disease progression. These findings highlight the pivotal role of the CCR7/NF-κB signaling pathway in AS-associated inflammation and present a translational nanotherapeutic strategy with the potential to overcome the clinical limitations of Col.</p> Graphical Abstract <p></p>

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

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年11月25日

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  • Qi Chen,
  • Yuan-Shu Peng,
  • Qian Zhong,
  • Yu-Bo Zhang,
  • Liu-Bing Hu,
  • Guan-Yan Zhang,
  • Yi-Xian Xu,
  • Pei-Na Dong,
  • Si Shen,
  • Jing-Hao Wang,
  • Zhi-Guo Wang,
  • Huan-Tian Zhang,
  • Rong Zeng,
  • Hao Wang

摘要

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, leading to a marked downregulation of pro-inflammatory cytokine and disruption of inflammatory cascades. In ApoE−/− AS mouse models, Col@PSVs treatment significantly improved plaque stability and attenuated disease progression. These findings highlight the pivotal role of the CCR7/NF-κB signaling pathway in AS-associated inflammation and present a translational nanotherapeutic strategy with the potential to overcome the clinical limitations of Col.

Graphical Abstract