doi: 10.1016/j.gca.2018.04.016 305 XuL.LiuT.LiuL.YaoX.ChenL.FanD.et al
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Its core molecular mechanisms involve the collapse of the antioxidant defense system, particularly the inactivation of glutathione peroxidase 4 (GPX4), inhibition of the cystine/glutamate antiporter (System Xc - ), and dysregulation of the ferroptosis suppressor protein 1 (FSP1) pathway ( - supports GPX4 function by maintaining the supply of cysteine and GSH, whereas FSP1 independently inhibits lipid peroxidation by reducing the level of ubiquinone (CoQ10), thereby preventing ferroptosis ( 2+ , thereby promoting ferroptosis and suppressing tumor growth ( The tumor immune microenvironment (TIME) of GBM is characterized by highly immunosuppressive characteristics, marked by the polarization of tumor-associated macrophages (TAMs) toward the M2 phenotype, T-cell functional exhaustion, excessive infiltration of regulatory T cells (Tregs), and high expression of the immune checkpoint molecules PD1/PD-L1 ( Figure 1 ) The unique TIME of GBM not only promotes tumor cell growth and invasion but also limits the efficacy of existing chemotherapy and radiotherapy ( + T-cell exhaustion and Treg enrichment further constrain cytotoxic T lymphocyte (CTL) activity, impairing antitumor immunity and facilitating immune escape ( Figure 1 Metabolic alterations are considered key drivers in regulating the suppressive TIME of GBM
In contrast to ALMT1-mediated GABA transport, the presence of Al 3+ blocks the influx of GABA from the apoplast to the cytoplasm during ALMT1 transport, while it does not affect the GABA transport facilitated by GAT1 (Long et al
Behets syndrome as a model of thrombo-inflammation: the role of neutrophils
