泌尿系统癌症中铁死亡与免疫系统之间的交互作用：机制、预后价值及治疗意义

Ferroptosis-an iron-dependent, lipid peroxidation-driven cell death-has emerged as a central regulator of tumor biology and antitumor immunity in prostate, bladder, and renal cancers. Beyond direct cytotoxicity, it bidirectionally reshapes the tumor immune microenvironment. CD8 + and NK cells induce ferroptosis via IFN-γ-mediated suppression of system Xc-, whereas ferroptotic cells release DAMPs and antigens that mature dendritic cells and activate T cells. Conversely, ferroptosis in effector lymphocytes and tumor antioxidant, metabolic, and myeloid programs can enforce immune suppression.

mRNA and lncRNA ferroptosis signatures stratify prognosis and immunotherapy response, often separating checkpoint-restrained "hot" tumors from immune-excluded/desert states. Mechanistic nodes (SLC7A11, GPX4, PRMT5, ATF4/NUPR1) and stromal/macrophage circuits link ferroptosis resistance to immune evasion. Emerging strategies combine ferroptosis induction with checkpoint blockade, adoptive cellular therapies, nano-delivery, and microenvironment reprogramming to convert "cold" disease into durable responders.