中国神经再生研究(英文版) ›› 2023, Vol. 18 ›› Issue (8): 1715-1716.doi: 10.4103/1673-5374.363197

• 观点:神经损伤修复保护与再生 • 上一篇    下一篇

神经炎性疾病中的神经血管单元通透性:一个共同的病理和治疗靶标?

  

  • 出版日期:2023-08-15 发布日期:2023-02-16

Neurovascular unit permeability in neuroinflammatory diseases: a common pathologic and therapeutic target?

Molly Monsour, Cesar V. Borlongan*   

  1. University of South Florida Morsani College of Medicine, Tampa, FL, USA (Monsour M);
    Department of Neurosurgery and Brain Repair, University of South Florida, Morsani College of Medicine, Tampa, FL, USA (Borlongan CV)
  • Online:2023-08-15 Published:2023-02-16
  • Contact: Cesar V. Borlongan, PhD, cborlong@usf.edu.

摘要: https://orcid.org/0000-0002-2966-9782 (Cesar V. Borlongan)

Abstract: Deleterious inflammatory cell invasion has been implicated in neurological diseases, partly manifesting as a leaky blood-central nervous system barrier (BCNSB) (Huang et al., 2021). Uncovering the perturbations of the neurovascular unit (NVU) may reveal the role of detrimental pro-inflammatory cells and signaling molecules in disrupting the central nervous system immune-privileged environment. The NVU includes the central nervous system, BCNSB, and surrounding vasculature, allowing for a tightly modulated exchange of oxygen and nutrients, while prohibiting unwanted peripheral signals (Iadecola, 2017). The protective properties of the NVU are reliant upon functional neurons, glial cells, endothelial cells, vascular smooth muscle cells, pericytes, and a basement membrane (Monsour et al., 2022). In numerous brain disease processes, such as amyotrophic lateral sclerosis (ALS), Alzheimer’s disease (AD), multiple sclerosis (MS), Parkinson’s disease (PD), ischemic stroke, and traumatic brain injury (TBI), the components of the NVU and their functions are impaired, resulting in a leaky BCNSB permitting inflammatory cell entry into the central nervous system (Table 1 and Figure 1).