胰腺癌是一种高度恶性的癌症，其与其他胃肠道肿瘤的区别在于显着的纤维化和独特的神经周围浸润。这些特征强调了胰腺癌肿瘤微环境（TME）内神经调节的复杂性。本综述旨在探讨胰腺癌微环境中基质细胞及其因子之间的调节机制和串扰。我们首先回顾胰腺癌微环境的主要组成部分，分析关键细胞类型（例如癌症相关成纤维细胞（CAF）和免疫细胞）之间的相互作用，并揭示肿瘤细胞与周围神经、免疫和基质细胞之间的动态变化。我们讨论神经生长因子（NGF）和脑源性神经营养因子（BDNF）等神经因子在胰腺癌进展中的作用，以及交感神经和副交感神经系统调节肿瘤细胞生长、迁移、转移的机制。和入侵。胰腺癌微环境中基质细胞、细胞因子和神经因子之间的相互作用促进纤维化和神经周围侵袭。更深入地了解胰腺癌微环境中各成分之间的调节和串扰，为抑制胰腺癌纤维化和神经周围侵袭提供了新的视角。版权所有© Bentham Science Publishers；如有任何疑问，请发送电子邮件至 epub@benthamscience.net。

Pancreatic cancer is a highly malignant form of cancer that distinguishes itself from other gastrointestinal tumors through significant fibrosis and unique perineural invasion. These characteristics underscore the complexity of neural regulation within the pancreatic cancer Tumor Microenvironment (TME). This review aimed to explore the regulatory mechanisms and crosstalk among stromal cells and their factors within the pancreatic cancer microenvironment. We begin by reviewing the major components of the pancreatic cancer microenvironment, analyzing interactions among crucial cell types, such as Cancer-associated Fibroblasts (CAFs) and immune cells, and revealing the dynamic changes between tumor cells and surrounding nerves, immune, and stromal cells. We discuss the role of neural factors, including the Nerve Growth Factor (NGF) and Brain-derived Neurotrophic Factor (BDNF), in the progression of pancreatic cancer and the mechanisms by which the sympathetic and parasympathetic nervous systems regulate tumor cell growth, migration, and invasion. Interactions among stromal cells, cytokines, and neural factors in the pancreatic cancer microenvironment promote fibrosis and perineural invasion. A deeper understanding of the regulation and crosstalk among components in the pancreatic cancer microenvironment offers new perspectives for inhibiting fibrosis and perineural invasion in pancreatic cancer.Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.