ReviewJournal of molecular medicine (Berlin, Germany)2026
The role of ferroptosis in renal cell carcinoma: molecular mechanisms and therapeutic implications.
Review in Journal of molecular medicine (Berlin, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed.
- LD-associated signatures identified by perilipin-based proximity labeling proteomics reveal GNA14 as a therapeutic and prognostic target in renal cell carcinoma.Cancer gene therapy · 2026Article
- The clinical landscape of HIF2α inhibitors in oncology.Nature reviews. Clinical oncology · 2026Review
- Mitochondrial Dysfunction in Renal Cell Carcinoma: A Comprehensive Review of Pathogenic Mechanisms and Emerging Therapeutic Opportunities.Oncology research · 2026Review
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Of the numerous regulatory cell death mechanisms, ferroptosis has emerged as a pivotal player in the pathobiology of renal cell carcinoma (RCC), particularly the clear-cell subtype (ccRCC). This iron-dependent form of cell death, characterized by the catastrophic accumulation of lipid peroxides, is intimately linked to the unique metabolic landscape of ccRCC, including its lipid-rich environment and reliance on specific antioxidant pathways. This review comprehensively synthesizes the current understanding of the molecular mechanisms governing ferroptosis in RCC. We delineate the core regulatory machinery, including the system xc-/GSH/GPX4 axis and key lipid-metabolizing enzymes like ACSL3 and ACSL4, and explore the multifaceted transcriptional, epigenetic, and metabolic networks that fine-tune ferroptotic sensitivity. Beyond summarizing established paradigms, this review places particular emphasis on the multilayer regulatory networks (including transcriptional, epigenetic, and metabolic rewiring) that fine-tune ferroptotic sensitivity, and critically examines the emerging role of ferroptosis suppression as a core mechanism of resistance to tyrosine kinase inhibitors. We also dissect the intricate crosstalk between ferroptosis and the tumor immune microenvironment, highlighting its impact on prognosis and immunotherapy response. Finally, we survey the evolving therapeutic landscape, encompassing small-molecule inducers, natural compounds, and innovative combination strategies designed to trigger ferroptosis. This comprehensive overview underscores ferroptosis as a critical vulnerability and a promising therapeutic target to overcome treatment resistance in RCC.
Indexed as
Identifiers
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.