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Preclinical studies reveal that VEGF-mediated vascular abnormalities not only impair drug delivery but also establish an immunosuppressive niche through multiple pathways: (1) upregulation of PD-L1/CTLA-4 expression on endothelial and immune cells (80, 81), (2) recruitment of regulatory T cells and myeloid-derived suppressor cells (32), and (3) induction of hypoxia-driven adenosine accumulation (82)

Importantly, this did not interfere with the capacity to isolate mitochondria from HA-Mito cells (Supplementary Fig

N-acetylcysteine (NAC) is a supplement that provides cysteine, often the scarcest ingredient required to make glutathione

GSH-dependent activation releases Cu + to engage lipoylated DLAT and simultaneously unmasks glucose oxidase activity, inducing nutrient deprivation and triggering cuproptosis 216