Kim Seunghee, Lee Minjae, Choi Yoon Kyung
Department of Bioscience and Biotechnology, Konkuk University, Seoul 05029, Republic of Korea.
Biomol Ther (Seoul). 2020 Jan 1;28(1):45-57. doi: 10.4062/biomolther.2019.119.
In the neurovascular unit, the neuronal and vascular systems communicate with each other. O and nutrients, reaching endothelial cells (ECs) through the blood stream, spread into neighboring cells, such as neural stem cells, and neurons. The proper function of neural circuits in adults requires sufficient O and glucose for their metabolic demands through angiogenesis. In a central nervous system (CNS) injury, such as glioma, Parkinson's disease, and Alzheimer's disease, damaged ECs can contribute to tissue hypoxia and to the consequent disruption of neuronal functions and accelerated neurodegeneration. This review discusses the current evidence regarding the contribution of oxygen deprivation to CNS injury, with an emphasis on hypoxia-inducible factor (HIF)-mediated pathways and Notch signaling. Additionally, it focuses on adult neurological functions and angiogenesis, as well as pathological conditions in the CNS. Furthermore, the functional interplay between HIFs and Notch is demonstrated in pathophysiological conditions.
在神经血管单元中,神经元和血管系统相互通信。氧气和营养物质通过血流到达内皮细胞(ECs),并扩散到邻近细胞,如神经干细胞和神经元。成体神经回路的正常功能需要通过血管生成来满足其代谢需求的充足氧气和葡萄糖。在中枢神经系统(CNS)损伤,如胶质瘤、帕金森病和阿尔茨海默病中,受损的内皮细胞会导致组织缺氧,进而破坏神经元功能并加速神经退行性变。本综述讨论了关于缺氧对中枢神经系统损伤作用的当前证据,重点关注缺氧诱导因子(HIF)介导的途径和Notch信号传导。此外,它还关注成体神经功能和血管生成,以及中枢神经系统的病理状况。此外,在病理生理条件下证明了HIFs和Notch之间的功能相互作用。