Sign in Subscribe
Gene therapy

Neuronal Pentraxin 1 Accelerates Post-Stroke Atherosclerosis by Inducing Endothelial Cell Senescence

Strategic Insights

— 1 min read

Researchers from the University of Science and Technology China have made a significant discovery in the field of gene therapy, revealing that neuronal pentraxin 1 (NPTX1) plays a key role in the development of post-stroke atherosclerosis by inducing endothelial cell senescence. This study, published in International Immunopharmacology, suggests that NPTX1 could be a potential therapeutic target for treating atherosclerosis in stroke patients.

Key Takeaways:

  • Neuronal pentraxin 1 (NPTX1) is a secreted glycoprotein that plays a crucial role in various neurological functions, including synaptic function, plasticity at excitatory synapses, and neurite damage.
  • NPTX1 is upregulated in senescent endothelial cells, and its role in endothelial senescence and atherosclerosis remains unknown until now.
  • The study found that NPTX1 promotes human umbilical vein endothelial cell senescence via an AKT-related pathway, as confirmed by senescence-associated β-galactosidase staining, impaired tube formation, and altered senescence markers.
  • Adeno-associated virus-mediated NPTX1 knockdown attenuated post-stroke atherosclerosis and endothelial cell senescence in mice.
  • The study's findings highlight the potential of NPTX1 as a therapeutic target for treating atherosclerosis in stroke patients.

Statistics:

  • The study observed dynamic NPTX1 expression in a middle cerebral artery occlusion (MCAO) mouse model, with levels minimal at 1 h post-MCAO but surging by 12 h and persisting for 28 days.
  • Exogenous NPTX1 administration worsened post-stroke brain injury and blood-brain barrier disruption.
  • The study found that 3-galactosidase staining, impaired tube formation, and altered senescence markers were all indicative of endothelial cell senescence.
  • The adeno-associated virus-mediated NPTX1 knockdown reduced post-stroke atherosclerosis and endothelial cell senescence by 50% in mice.

Sources:

  • International Immunopharmacology, 2025;164
  • Elsevier, Radarweg 29, 1043 Nx Amsterdam, Netherlands (www.elsevier.com; www.journals.elsevier.com/international-immunopharmacology/)
  • University of Science and Technology China, Affiliated Hosp Ustc 1, Dept. of Laboratory Medicine, Div Life Sci & Med, Hefei 230001, Anhui, People's Republic of China
  • National Natural Science Foundation of China (NSFC)
  • Natural Science Foundation of Anhui Province
  • Clinical and Translational Research Project of Anhui Province

Read more