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嘌呤能信号在少突胶质细胞发育和髓鞘修复中的作用及机制研究进展

The role and mechanism of purinergic signaling in oligodendrocytes development and myelin repair:A literature review
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摘要 少突胶质细胞(OL)是发育中的中枢神经系统(central nervous system,CNS)髓鞘形成和髓鞘损伤再生的关键;ATP不仅是一种能量载体,也作为一个重要的信号分子参与细胞之间的交流,其嘌呤能受体亚型广泛存在于神经元和神经胶质细胞中,主要包括接受腺苷信号的P1受体和接受ATP/ADP/UTP信号的P2受体。不同亚型的嘌呤能受体在CNS中不同部位的表达及其在生理病理状态下发挥的具体作用和机制也各有不同,本文对近年来关于嘌呤能受体在OL发育及髓鞘形成与修复中作用和机制研究的新进展进行综述,该方面的研究对于了解嘌呤能信号在诸多脱髓鞘性疾病以及髓鞘发育障碍性疾病中的作用、发掘相应的潜在治疗靶点具有重要的意义。 Oligodendrocytes(OLs)play a crucial role in myelination during the development and repair of the central nervous system.ATP serves not only as an important signaling molecule involving in the intercellular com-munications,but also as an energetic molecule,with its purinergic receptor subtypes widely present in neurons and glial cells.These subtypes are composed of two purinergic receptors:P1 and P2:The former are primarily activated by adenosine,and the latter mainly by ATP,ADP,and UTP.The two receptors paly their respective role in various regions of the CNS under physiological or pathological conditions through distinct mechanisms.In this paper,we review recent literature on the roles and mechanisms of the purinergic receptors in OL development,myelination,and myelin repair.It may be of great significance for further understanding the role of purinergic signaling in demy-elinating diseases and myelin dysplasia and exploring potential therapeutic targets.
作者 何月华 谢华 肖林 HE Yuehua;XIE Hua;XIAO Lin(Key Laboratory of Brain,Cognition and Education Sciences of Ministry of Education,Institute for Brain Research and Rehabilitation,Guangdong Key Laboratory of Mental Health and Cognitive Science,and Center for Studies of Psychological Application,South China Normal University,Guang-zhou 510631,China)
出处 《实用医学杂志》 CAS 北大核心 2024年第5期714-720,共7页 The Journal of Practical Medicine
基金 中国科技创新重大项目(编号:2021ZD0201703) 国家自然科学基金(编号:31970913,32170957) 广东省基础与应用基础研究基金(编号:2021A1515012156) 广东省重点领域研发计划(编号:2019B030335001)。
关键词 ATP 嘌呤能受体 少突胶质细胞 髓鞘形成 髓鞘修复 ATP purinergic receptor oligodendrocyte myelination myelin repair
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