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Ferroptosis is a form of regulated cell death driven by labile iron-dependent lipid peroxidation and is closely integrated with cellular energy metabolism and redox homeostasis. Once viewed primarily as the terminal product of glycolysis, lactate is now recognized as a central metabolic intermediate, signaling molecule, and epigenetic substrate that reshapes intracellular and microenvironmental redox networks and thereby influences cell fate. Emerging evidence suggests that lactate exerts a context-dependent and bidirectional influence on the ferroptosis machinery. This regulation is mediated through four closely interconnected dimensions: lactate flux and concentration gradients, extracellular acidosis within the microenvironment, monocarboxylate transporter (MCT)-dependent transmembrane metabolic exchange, and site-specific histone and non-histone lactylation. This review systematically examines how lactate regulates ferroptosis in a context-dependent manner across different cell types, subcellular compartments, and disease microenvironments. In many tumors and stromal niches, lactate can act as a metabolic barrier that supports immunosuppression and ferroptosis resistance. By contrast, under specific stress conditions, dysregulated lactate flux may promote metabolic imbalance, epigenetic reprogramming, and increased ferroptotic vulnerability. We further summarize recent translational advances targeting the lactate-ferroptosis axis, including compartment-specific pharmacological strategies, emerging nanomedicine-based delivery platforms, and physical approaches for modulating the microenvironment. Although this framework provides a useful basis for therapeutic exploration, most current evidence remains preclinical. Rigorous validation in human tissues, patient-derived models, and early-phase clinical studies will be required before lactate-targeted ferroptosis strategies can be advanced toward precision therapy.