N-甲基-D-天冬氨酸受体在胰腺导管腺癌神经侵犯中的作用研究进展
Advances in the Role of N-Methyl-D-Aspartate Receptor in Perineural Invasion of Pancreatic Ductal Adenocarcinoma
DOI: 10.12677/acm.2026.1652031, PDF,    科研立项经费支持
作者: 刘常乐, 王乃赓, 任建军*:内蒙古医科大学附属医院肝胆外科,内蒙古 呼和浩特;肖 瑞:内蒙古医科大学分子病理学重点实验室,内蒙古 呼和浩特
关键词: 胰腺导管腺癌N-甲基-D-天冬氨酸受体神经侵犯治疗靶点Pancreatic Ductal Adenocarcinoma N-Methyl-D-Aspartate Receptor Perineural Invasion Therapeutic Target
摘要: 胰腺导管腺癌(Pancreatic Ductal Adenocarcinoma, PDAC)预后极差,神经侵犯(Perineural Invasion, PNI)是其重要病理特征,与患者疼痛和不良预后密切相关。N-甲基-D-天冬氨酸受体(N-methyl-D-aspartate receptor, NMDAR)作为离子型谷氨酸受体的重要成员,近年来被证实在肿瘤PNI过程中发挥关键作用。该文章综述了NMDAR促进胰腺导管腺癌PNI的主要机制:激活Ca2+信号通路、介导伪突触形成、调控施万细胞代谢重塑。深入研究NMDAR在胰腺导管腺癌PNI中的作用机制,可为胰腺癌治疗提供新的干预靶点和治疗策略。
Abstract: Pancreatic ductal adenocarcinoma (PDAC) has an extremely poor prognosis. Perineural invasion (PNI) is a key pathological feature of PDAC and is closely associated with patient pain and unfavorable outcomes. As a crucial member of the ionotropic glutamate receptors, the N-methyl-D-aspartate receptor (NMDAR) has recently been demonstrated to play a pivotal role in tumor PNI. This article reviews the main mechanisms by which NMDAR promotes PNI in PDAC: activating Ca2+ signaling pathways, mediating pseudo-synapse formation, and regulating Schwann cell metabolic remodeling. In-depth investigation into the mechanisms of NMDAR in PNI of PDAC may provide novel intervention targets and therapeutic strategies for pancreatic cancer treatment.
文章引用:刘常乐, 肖瑞, 王乃赓, 任建军. N-甲基-D-天冬氨酸受体在胰腺导管腺癌神经侵犯中的作用研究进展[J]. 临床医学进展, 2026, 16(5): 2219-2223. https://doi.org/10.12677/acm.2026.1652031

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