Lu Rongze Olivia, Ho Winson S
Department of Neurosurgery, Dell Medical School, University of Texas at Austin, Austin, TX, United States.
Mulva Clinic for the Neurosciences, Dell Medical School, University of Texas at Austin, Austin, TX, United States.
Front Cell Dev Biol. 2021 Jan 15;8:620788. doi: 10.3389/fcell.2020.620788. eCollection 2020.
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进展中起关键作用，因为线粒体在调节细胞代谢、氧化应激和细胞死亡方面至关重要。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）为主导，TAM是一群异质性的髓样细胞，通常会营造一种免疫抑制环境以支持肿瘤生长。然而，TAM的某些亚群可能具有促炎作用，从而起到抗肿瘤作用。针对TAM的治疗策略正越来越多地被探索作为GBM的新型治疗策略。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在塑造肿瘤免疫微环境过程中介导胶质瘤线粒体功能障碍与TAM表型相互作用的可能分子机制。
