神经胶质瘤是起源于中枢神经系统的原发性肿瘤。神经胶质瘤的常规治疗选择通常包括手术切除和替莫唑胺（TMZ）化疗。然而，尽管采取了积极的干预措施，神经胶质瘤患者的中位生存期仅为约 14.6 个月。因此，迫切需要探索治疗神经胶质瘤的创新治疗策略。调节性细胞死亡 (RCD) 的基础研究可以追溯到 Karl Vogt 对蟾蜍细胞死亡的开创性观察，该观察于 1842 年记录在案。在过去的十年中，细胞死亡命名委员会 (NCCD) 对细胞死亡进行了系统的分类和描述。细胞死亡的各种形式和机制，综合形态、生化和功能特征。细胞死亡主要表现为两种形式：意外细胞死亡（ACD），由物理、化学或机械破坏等外部因素引起； RCD，一种基因引导的内在过程，协调有序的细胞死亡以响应生理和病理线索。我们对 RCD 理解的进步揭示了细胞死亡调节的操纵（通过诱导或抑制）作为肿瘤学中潜在的突破性方法，具有重大前景。然而，研究和临床应用之间仍然存在障碍，在转化为治疗方式方面遇到了重大障碍。越来越明显的是，对细胞死亡的分子基础进行综合检查对于推进该领域至关重要，特别是在途径间功能协同的框架内。在这篇综述中，我们概述了各种形式的 RCD，包括自噬依赖性细胞死亡、失巢凋亡、铁死亡、铜死亡、焦亡和免疫原性细胞死亡。我们总结了了解调节神经胶质瘤 RCD 的分子机制的最新进展，并探讨了不同细胞死亡过程之间的相互联系。通过理解这些联系并制定有针对性的策略，我们有潜力通过操纵 RCD 来增强神经胶质瘤的治疗。版权所有 © 2024 Luo、Luan、Yang、Chen、Yuan、Cao、Zhang、Xie、Luo、Chen、Li、Xiang 和 Zhou 。

Gliomas are primary tumors that originate in the central nervous system. The conventional treatment options for gliomas typically encompass surgical resection and temozolomide (TMZ) chemotherapy. However, despite aggressive interventions, the median survival for glioma patients is merely about 14.6 months. Consequently, there is an urgent necessity to explore innovative therapeutic strategies for treating glioma. The foundational study of regulated cell death (RCD) can be traced back to Karl Vogt's seminal observations of cellular demise in toads, which were documented in 1842. In the past decade, the Nomenclature Committee on Cell Death (NCCD) has systematically classified and delineated various forms and mechanisms of cell death, synthesizing morphological, biochemical, and functional characteristics. Cell death primarily manifests in two forms: accidental cell death (ACD), which is caused by external factors such as physical, chemical, or mechanical disruptions; and RCD, a gene-directed intrinsic process that coordinates an orderly cellular demise in response to both physiological and pathological cues. Advancements in our understanding of RCD have shed light on the manipulation of cell death modulation - either through induction or suppression - as a potentially groundbreaking approach in oncology, holding significant promise. However, obstacles persist at the interface of research and clinical application, with significant impediments encountered in translating to therapeutic modalities. It is increasingly apparent that an integrative examination of the molecular underpinnings of cell death is imperative for advancing the field, particularly within the framework of inter-pathway functional synergy. In this review, we provide an overview of various forms of RCD, including autophagy-dependent cell death, anoikis, ferroptosis, cuproptosis, pyroptosis and immunogenic cell death. We summarize the latest advancements in understanding the molecular mechanisms that regulate RCD in glioma and explore the interconnections between different cell death processes. By comprehending these connections and developing targeted strategies, we have the potential to enhance glioma therapy through manipulation of RCD.Copyright © 2024 Luo, Luan, Yang, Chen, Yuan, Cao, Zhang, Xie, Luo, Chen, Li, Xiang and Zhou.