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Renal cell carcinoma (RCC) exhibits marked heterogeneity in its molecular landscape and clinical behavior. Ferroptosis, an iron-dependent and lipid peroxidation-driven form of cell death, has emerged as a biologically relevant process in RCC pathogenesis. This review summarizes recent advances in the multi-omics dissection of ferroptosis in RCC, including findings from genomics, epigenomics, transcriptomics, proteomics, metabolomics, and microbiomics. Key molecular regulators such as VHL, SLC7A11, GPX4, and ACSL4 are highlighted for their roles in ferroptosis sensitivity or resistance. In parallel, insights from single-cell and spatial omics offer new perspectives on cell-type specificity and microenvironmental context. We also discuss the implications of ferroptosis in therapeutic modulation, including potential integration with immune checkpoint inhibitors and metabolic interventions. This review aims to provide a coherent overview of ferroptosis in RCC and inform future mechanistic studies and translational strategies.
Wang et al. (Mon,) studied this question.