Glioblastoma (GBM) is the most common malignant brain cancer. Increasing evidence suggests that mitochondrial dysfunction plays a key role in GBM progression as mitochondria is essential in regulating cell metabolism, oxidative stress, and cell death. Meanwhile, the immune microenvironment in GBM is predominated by tumor-associated macrophages and microglia (TAM), which is a heterogenous population of myeloid cells that, in general, create an immunosuppressive milieu to support tumor growth. However, subsets of TAMs can be pro-inflammatory and thereby antitumor. Therapeutic strategies targeting TAMs are increasingly explored as novel treatment strategies for GBM. The connection between mitochondrial dysfunction and TAMs phenotype in the tumor microenvironment is unclear. This review aims to provide perspectives and discuss possible molecular mechanisms mediating the interplay between glioma mitochondrial dysfunction and TAMs phenotype in shaping tumor immune microenvironment.

胶质母细胞瘤（GBM）是最常见的恶性脑癌。越来越多的证据表明，线粒体功能障碍在 GBM 进展中发挥着关键作用，因为线粒体对于调节细胞代谢、氧化应激和细胞死亡至关重要。与此同时，GBM 中的免疫微环境以肿瘤相关巨噬细胞和小胶质细胞 (TAM) 为主，TAM 是骨髓细胞的异质群体，通常会创建一个免疫抑制环境来支持肿瘤生长。然而，TAM 的子集可能具有促炎作用，从而具有抗肿瘤作用。针对 TAM 的治疗策略越来越多地被探索作为 GBM 的新治疗策略。肿瘤微环境中线粒体功能障碍与 TAM 表型之间的联系尚不清楚。本综述旨在提供观点并讨论介导神经胶质瘤线粒体功能障碍和 TAM 表型之间相互作用在塑造肿瘤免疫微环境中的可能分子机制。