The occurrence and development of tumors involve a series of life activities of cells, among which cell death has always been a crucial part in the research of tumor mechanisms and treatment methods. Ferroptosis is a non-apoptotic form of cell death, which is characterized by lipid peroxidation accumulation and further cell membrane rupture caused by excessive production of intracellular oxygen free radicals dependent on iron ions. Esophageal cancer is one of the common digestive tract tumors. Patients in the early stage are mainly treated with surgery, and the curative effect is awe-inspiring. However, surgery is far from enough for terminal patients, and it is the best choice to combine radiotherapy and chemotherapy before the operation or during the perioperative period. Although the treatment plan for patients with advanced esophageal cancer is constantly being optimized, we are disappointed at the still meager 5-year survival rate of patients and the poor quality of life. A series of complex problems, such as increased chemotherapy drug resistance and decreased radiotherapy sensitivity of esophageal cancer cells, are waiting for us to tackle. Perhaps ferroptosis can provide practical and feasible solutions and bring new hope to patients with advanced esophageal cancer. The occurrence of ferroptosis is related to the dysregulation of iron metabolism, lipid metabolism, and glutamate metabolism. Therefore, these dysregulated metabolic participant proteins and signaling pathways are essential entry points for using cellular ferroptosis to resist the occurrence and development of cancer cells. This review first introduced the main regulatory mechanisms of ferroptosis. It then summarized the current research status of ferroptosis in esophageal cancer, expecting to provide ideas for the research related to ferroptosis in esophageal cancer.