自噬是一种正常的生理过程，有助于细胞营养物质的循环利用，帮助细胞应对应激条件。然而，自噬对包括神经胶质瘤在内的癌症的影响尚不确定，并且涉及复杂的分子机制。一些相互矛盾的报告表明自噬可能促进或抑制神经胶质瘤的生长和进展。自噬抑制剂可增强胶质瘤化疗或放疗的疗效。许多化合物刺激自噬导致神经胶质瘤细胞死亡。自噬也参与神经胶质瘤的治疗抵抗。本文旨在阐明自噬复杂的分子机制，以更好地理解自噬在胶质瘤中的双向作用及其治疗意义。本文描述了自噬的细胞保护和细胞毒性作用的蛋白质和表观遗传调节剂。此外，一些信号通路与自噬及其对神经胶质瘤的影响有关。我们回顾了分子途径并强调了细胞保护和细胞毒性自噬中涉及的信号轴。此外，本文讨论了自噬在治疗抵抗中的作用，包括神经胶质瘤干细胞维持和肿瘤微环境调节。它还总结了关于自噬调节剂的抗神经胶质瘤作用的多项研究，以了解相关机制并提供有关其治疗意义的见解。版权所有 © 2024 Elsevier B.V. 保留所有权利。

Autophagy is a normal physiological process that aids the recycling of cellular nutrients, assisting the cells to cope with stressed conditions. However, autophagy's effect on cancer, including glioma, is uncertain and involves complicated molecular mechanisms. Several contradictory reports indicate that autophagy may promote or suppress glioma growth and progression. Autophagy inhibitors potentiate the efficacy of chemotherapy or radiation therapy in glioma. Numerous compounds stimulate autophagy to cause glioma cell death. Autophagy is also involved in the therapeutic resistance of glioma. This review article aims to detangle the complicated molecular mechanism of autophagy to provide a better perception of the two-sided role of autophagy in glioma and its therapeutic implications. The protein and epigenetic modulators of the cytoprotective and cytotoxic role of autophagy are described in this article. Moreover, several signaling pathways are associated with autophagy and its effects on glioma. We have reviewed the molecular pathways and highlighted the signaling axis involved in cytoprotective and cytotoxic autophagy. Additionally, this article discusses the role of autophagy in therapeutic resistance, including glioma stem cell maintenance and tumor microenvironment regulation. It also summarizes several investigations on the anti-glioma effects of autophagy modulators to understand the associated mechanisms and provide insights regarding its therapeutic implications.Copyright © 2024 Elsevier B.V. All rights reserved.