<p>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.</p> Graphical Abstract <p></p>