应激无处不在,而感知应激并调节身体机能以应对危险,是生命体生存的重要机制。然而过度或长期的应激则会发展成焦虑(anxiety),损害生物体的健康。近年来大量研究表明,应激和焦虑会促进肿瘤的发生发展。它们主要通过激活交感神经系统(sympathetic nervous system)释放相关的激素或外周神经递质,激活肿瘤细胞及微环境上的相关受体促进肿瘤的增殖、生存及血管生成,导致肿瘤进展的加速,同时也损害机体的免疫反应,使肿瘤细胞逃脱免疫系统的“监控”。然而应激感知和焦虑反应相关的神经环路如何通过交感神经系统与肿瘤关联并影响肿瘤发生发展的确切机制尚不清楚。本文就焦虑相关神经系统网络与交感神经系统的连接及交感系统对肿瘤的影响途径进行总结综述,为未来癌症的治疗奠定理论依据。

Stress can be found almost anywhere. Perceiving stress and regulating bodily functions to respond to danger constitute crucial mechanisms on which individuals rely for their survival. However, excessive or chronic stress can lead to the development of anxiety, posing a threat to individuals’ health. In recent years, many studies have indicated that stress and anxiety can promote the initiation and progression of cancer. These effects are primarily operated through the activation of the sympathetic nervous system, resulting in the release of relevant hormones or peripheral neurotransmitters. This process triggers the promotion of cell proliferation, survival, and angiogenesis by activating the relevant receptors on both tumor cells and the microenvironment. Consequently, it accelerates cancer progression. Simultaneously, it compromises the body 's immune response, enabling tumor cells to evade immune surveillance. Nonetheless, the precise mechanisms underlying how the neural circuits associated with stress perception and anxiety response are interconnected with tumors and influence the occurrence and development of tumors through the sympathetic nervous system remain unclear. This article surveys a comprehensive overview and summary of the connections between anxiety-related neural systems and the sympathetic nervous system, as well as the pathways through which the sympathetic nervous system affects tumors, laying the theoretical foundation for future cancer treatments.