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Radiotherapy increases tumor cell ferroptosis susceptibility, significantly inducing the expression of long-chain acyl-CoA synthetase 4 (ACSL4) and the ferroptosis inhibitors SLC7A11 and GPX4, thereby effectively suppressing tumor growth ( Researchers successfully repolarized macrophages from tumor-promoting M2 to anti-tumor M1 phenotype through ferroptosis using MIL88B/RSL3 nanomaterials
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BPC-157 modulates inflammatory cascades through effects on the erg-1 transcription factor and prostaglandin systems
Figure 6 Moreover, up-regulated DEPs were found to be enriched in antigen processing and presentation, human immunodeficiency virus 1 infection, herpes simplex virus 1 infection, acute myeloid leukemia, etc
This interaction promotes M2 macrophage polarization, enhancing pro-tumorigenic phenotypes ( 4.3 Macrophage-ferroptosis immunometabolism Tumor-associated macrophages (TAMs) and ferroptotic cancer cells engage in a highly integrated, bidirectional metabolic dialogue that shapes immune outcomes and determines tumor ( + , increased transferrin receptor (TfR1) expression, and restricted ferroportin activity, thereby enriching the tumor microenvironment (TME) with redox-active iron ( Ferroptotic cancer cells reciprocally influence macrophage states by releasing DAMPs (HMGB1), oxidized phosphatidylethanolamines (SAPE-OOH), iron-loaded vesicles, and lipid peroxidation products that serve as signals to recruit, polarize, or reprogram macrophages ( Figure 5
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