Abstract: Non-alcoholic fatty liver disease (NAFLD) is the most prevalent chronic liver disease globally, with its incidence rate continuously rising and showing a trend of affecting younger populations. Recent studies have revealed that autophagy and ferroptosis form a critical crosstalk network via the mitochondrial autophagy receptor FUNDC1, and their imbalance constitutes the core mechanism underlying the progression of NAFLD. Both research and guidelines emphasize the pathogenic role of ferroptosis in non-alcoholic steatohepatitis (NASH) and list ferroptosis inhibitors (such as Liproxstatin-1) as important targets in phase Ⅱ clinical trials. Metabolic and bariatric surgery (such as sleeve gastrectomy) can restore the balance between autophagy and ferroptosis by upregulating FUNDC1 and inhibiting the HIF-1α/NOX4 pathway, significantly improving iron overload, lipid peroxidation, and insulin resistance. Multi-center clinical and animal experiments have confirmed that the decline in ferroptosis markers (4-HNE, ferritin) after surgery is significantly associated with improvements in HOMA-IR and HbA1c, and the combination with ferroptosis inhibitors can synergistically enhance the repair of insulin signaling pathways. This article systematically reviewed the regulatory mechanisms and intervention strategies of this molecular axis, providing a theoretical basis for the precise treatment of NAFLD.