中国神经再生研究(英文版) ›› 2021, Vol. 21 ›› Issue (5): 2005-2006.doi: 10.4103/NRR.NRR-D-24-01619

• 观点:神经损伤修复保护与再生 • 上一篇    下一篇

脂肪组织来源细胞外囊泡在血管炎症和功能障碍中的作用与机制

  

  • 出版日期:2026-05-15 发布日期:2025-08-22

Effects and mechanisms of adipose tissue–derived extracellular vesicles in vascular inflammation and dysfunction

Daphne Lintsen, Bieke Broux*   

  1. University MS Center, Campus Diepenbeek, Diepenbeek, Belgium (Lintsen D, Broux B) Neuro-Immune Connections and Repair Lab, Department of Immunology and Infection, Biomedical Research Institute, Hasselt University, Diepenbeek, Belgium (Lintsen D, Broux B)
  • Online:2026-05-15 Published:2025-08-22
  • Contact: Bieke Broux, PhD, Bieke.broux@uhasselt.be.
  • Supported by:
    We would like to thank Kenneth Verboven (Hasselt University, Belgium), Kristiaan Wouters (Maastricht University, The Netherlands), Lisa Schütz (Hasselt University, Belgium and Maastricht University, The Netherlands), and Lisa Mennens (Hasselt University, Belgium and Maastricht University, The Netherlands) for fruitful discussions. This work was supported by FWO (Fonds voor Wetenschappelijk Onderzoek), grant number G07562NFWO (to BB).

摘要: https://orcid.org/0000-0001-8509-2415 (Bieke Broux)

Abstract: Neuroinflammation is a key process in the pathogenesis of various neurodegenerative diseases, such as multiple sclerosis (MS), Alzheimer ’s disease, and traumatic brain injury. Even for disorders historically unrelated to neuroinflammation, such as Alzheimer ’s disease, it is now shown to precede pathological protein aggregations. A common factor in these neurodegenerative diseases is activation of brain resident immune cells, as well as breakdown of the blood–brain barrier (BBB), which consecutively causes infiltration of peripheral immune cells, leading to neuronal damage and dysfunction. The integrity of the BBB, a biological barrier between the blood and the central nervous system, therefore plays a crucial role in regulating neuroinflammation. The BBB primarily consists of endothelial cells (ECs) that are tightly connected by tight junction proteins, astrocyte-end feet, and pericytes, conjunctively restricting the infiltration of immune cells and unnecessary biological molecules into the brain. BBB disruption, marked by the loss of structural integrity and upregulation of adhesion molecules and chemokines on the microvascular ECs, leads to infiltrating immune cells in the brain, driving neuroinflammation (Naegele and Martin, 2014).