Exploring immune-endothelial interactions in neuroinflammation and vascular dysfunction.
- 1Changchun University of Chinese Medicine, Changchun, China.
- 2Affiliated Hospital of Changchun University of Chinese Medicine, Changchun, China.
- 3Department of Biology, University of Pennsylvania, Philadelphia, PA, United States.
Abstract
Neuroinflammation and cerebrovascular endothelial dysfunction are traditionally studied as parallel processes confined to individual disease categories. Yet a growing body of evidence indicates that they operate as components of a tightly coupled, self-amplifying circuit: the immune-endothelial-neural axis. Within this axis, the peripheral immune system, cerebrovascular endothelium, and neural networks continuously modulate one another across disease contexts. This Review summarizes current knowledge on the bidirectional immune-endothelial interactions that underlie blood-brain barrier disruption and neuroinflammation across cerebrovascular disorders, neuroimmune diseases, and neurodegenerative conditions. A systems-level comparison across disease categories identifies shared pathological hallmarks alongside disease-specific signatures of tempo, vascular scale, and regional vulnerability. Emerging therapeutic strategies are considered along the three limbs of the axis: immunomodulation, endothelial protection and barrier stabilization, and neural recovery, including traditional Chinese medicine as a multitarget approach. By framing neurological disorders through the immune-endothelial-neural axis, this Review proposes a unifying framework that bridges disease boundaries and identifies common mechanistic targets for future translational research. The framework is offered as a testable proposition in which the relative contribution of each limb differs between disorders.
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BibTeX
@article{wang2026exploring,
title = {{Exploring immune-endothelial interactions in neuroinflammation and vascular dysfunction.}},
author = {Zitian Wang and Zezheng Kang and Lei Wu and Jinglin Hu and Xinhua Chen and Tuoxian Tang},
journal = {Frontiers in molecular neuroscience},
year = {2026},
month = oct,
doi = {10.3389/fnmol.2026.1978704},
url = {https://europepmc.org/article/MED/42953005},
note = {CC BY},
}
RIS
TY - JOUR
TI - Exploring immune-endothelial interactions in neuroinflammation and vascular dysfunction.
AU - Zitian Wang
AU - Zezheng Kang
AU - Lei Wu
AU - Jinglin Hu
AU - Xinhua Chen
AU - Tuoxian Tang
PY - 2026
DA - 2026/10/14
JO - Frontiers in molecular neuroscience
DO - 10.3389/fnmol.2026.1978704
UR - https://europepmc.org/article/MED/42953005
AB - Neuroinflammation and cerebrovascular endothelial dysfunction are traditionally studied as parallel processes confined to individual disease categories. Yet a growing body of evidence indicates that they operate as components of a tightly coupled, self-amplifying circuit: the immune-endothelial-neural axis. Within this axis, the peripheral immune system, cerebrovascular endothelium, and neural networks continuously modulate one another across disease contexts. This Review summarizes current knowledge on the bidirectional immune-endothelial interactions that underlie blood-brain barrier disruption and neuroinflammation across cerebrovascular disorders, neuroimmune diseases, and neurodegenerative conditions. A systems-level comparison across disease categories identifies shared pathological hallmarks alongside disease-specific signatures of tempo, vascular scale, and regional vulnerability. Emerging therapeutic strategies are considered along the three limbs of the axis: immunomodulation, endothelial protection and barrier stabilization, and neural recovery, including traditional Chinese medicine as a multitarget approach. By framing neurological disorders through the immune-endothelial-neural axis, this Review proposes a unifying framework that bridges disease boundaries and identifies common mechanistic targets for future translational research. The framework is offered as a testable proposition in which the relative contribution of each limb differs between disorders.
SN - 1662-5099
ER -