4.7 Article

The NG2-glia is a potential target to maintain the integrity of neurovascular unit after acute ischemic stroke

期刊

NEUROBIOLOGY OF DISEASE
卷 180, 期 -, 页码 -

出版社

ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.nbd.2023.106076

关键词

NG2-glia; Stroke; Neurovascular unit; Neurological functional recovery

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In this review, the critical role of NG2-glia in regulating NVU after AIS is discussed. The interactions between NG2-glia and other cells of NVU are emphasized, as well as the role of NG2-glia in oligodendrogenesis, white matter repair, and angiogenesis after AIS. Strategies to promote NG2-glia proliferation and differentiation are also reviewed, with the proposal of using DPSC-derived exosomes as a promising strategy for reducing AIS-induced injury and promoting repair.
The neurovascular unit (NVU) plays a critical role in health and disease. In the current review, we discuss the critical role of a class of neural/glial antigen 2 (NG2)-expressing glial cells (NG2-glia) in regulating NVU after acute ischemic stroke (AIS). We first introduce the role of NG2-glia in the formation of NVU during development as well as aging-induced damage to NVU and accompanying NG2-glia change. We then discuss the reciprocal interactions between NG2-glia and the other component cells of NVU, emphasizing the factors that could in-fluence NG2-glia. Damage to the NVU integrity is the pathological basis of edema and hemorrhagic trans-formation, the most dreaded complication after AIS. The role of NG2-glia in AIS-induced NVU damage and the effect of NG2-glia transplantation on AIS-induced NVU damage are summarized. We next discuss the role of NG2-glia and the effect of NG2-glia transplantation in oligodendrogenesis and white matter repair as well as angio-genesis which is associated with the outcome of the patients after AIS. Finally, we review the current strategies to promote NG2-glia proliferation and differentiation and propose to use the dental pulp stem cells (DPSC)-derived exosome as a promising strategy to reduce AIS-induced injury and promote repair through maintaining the integrity of NVU by regulating endogenous NG2-glia proliferation and differentiation.

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