Microglia-mediated inflammatory destruction of neuro-cardiovascular dysfunction after stroke

Jiahong Deng; Chenghan Chen; Shuaishuai Xue; Daoqing Su; Wai Sang Poon; Honghao Hou; Jun Wang

doi:10.3389/fncel.2023.1117218

Microglia-mediated inflammatory destruction of neuro-cardiovascular dysfunction after stroke

Front Cell Neurosci. 2023 Mar 21:17:1117218. doi: 10.3389/fncel.2023.1117218. eCollection 2023.

Authors

Jiahong Deng^{1

2

3}, Chenghan Chen^{1

2

3}, Shuaishuai Xue^{1

2

3}, Daoqing Su⁴, Wai Sang Poon⁵, Honghao Hou⁶, Jun Wang^{1

2

3}

Affiliations

¹ Department of Neurosurgery, Nanfang Hospital, Southern Medical University, Guangzhou, China.
² The First School of Clinical Medicine, Southern Medical University, Guangzhou, China.
³ Neural Networks Surgery Team, Southern Medical University, Guangzhou, China.
⁴ Department of Neurosurgery, The First Affiliated Hospital of Fujian Medical University, Fuzhou, Fujian, China.
⁵ Neuro-Medicine Center, The University of Hong Kong-Shenzhen Hospital, Shenzhen, China.
⁶ Guangdong Provincial Key Laboratory of Construction and Detection in Tissue Engineering, School of Basic Medical Science, Southern Medical University, Guangzhou, China.

Abstract

Stroke, a serious systemic inflammatory disease, features neurological deficits and cardiovascular dysfunction. Neuroinflammation is characterized by the activation of microglia after stroke, which disrupts the cardiovascular-related neural network and the blood-brain barrier. Neural networks activate the autonomic nervous system to regulate the cardiac and blood vessels. Increased permeability of the blood-brain barrier and the lymphatic pathways promote the transfer of the central immune components to the peripheral immune organs and the recruitment of specific immune cells or cytokines, produced by the peripheral immune system, and thus modulate microglia in the brain. In addition, the spleen will also be stimulated by central inflammation to further mobilize the peripheral immune system. Both NK cells and Treg cells will be generated to enter the central nervous system to suppress further inflammation, while activated monocytes infiltrate the myocardium and cause cardiovascular dysfunction. In this review, we will focus on microglia-mediated inflammation in neural networks that result in cardiovascular dysfunction. Furthermore, we will discuss neuroimmune regulation in the central-peripheral crosstalk, in which the spleen is a vital part. Hopefully, this will benefit in anchoring another therapeutic target for neuro-cardiovascular dysfunction.

Keywords: cardiac; inflammation; microglia; neural-network; spleen; stroke.

Publication types

Review

Grants and funding

This study was supported by grants from the Natural Science Fund of Guangdong Province (2017A030313597), the Natural Science Fund of Guangzhou in Basic and Applied Research (202201010875), and the Southern Medical University (S202012121088S, X202012121354, 202212121027, and S202212121113S).