ReviewMolecular cancer2026
Ferroptosis-autophagy crosstalk in bladder cancer: mechanisms and therapeutic implications.
Review in Molecular cancer, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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.
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3 authors.
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Abstract
Bladder cancer (BC) continues to be a prevalent malignancy within the urinary tract, characterized by high rates of recurrence, metastatic progression, and resistance to therapy, highlighting the importance of developing treatments that target regulated cell death pathways. Ferroptosis is a regulated form of cell death that depends on iron and is caused by excessive lipid peroxidation, whereas autophagy is a conserved catabolic process that can either buffer cellular stress or contribute to cell demise depending on context. Emerging evidence indicates that ferroptosis and autophagy intersect through shared metabolic and signaling nodes, including iron handling, glutathione and lipid metabolism, and stress-response pathways. In this narrative review, we summarize bladder-cancer-specific studies linking ferroptosis and autophagy, integrate mechanistic insights with evidence from patient cohorts and public datasets, and discuss translational opportunities and limitations for targeting this crosstalk in BC.
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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 Socratic graph.