Abnormal activation of ferroptosis worsens the severity of acute pancreatitis and intensifies the inflammatory response and organ damage, but the detailed underlying mechanisms are unknown. Compared with other types of pancreatitis, hyperlipidemic acute pancreatitis (HLAP) is more likely to progress to necrotizing pancreatitis, possibly due to peripancreatic lipolysis and the production of unsaturated fatty acids. Moreover, high levels of unsaturated fatty acids undergo lipid peroxidation and trigger ferroptosis to further exacerbate inflammation and worsen HLAP. This paper focuses on the malignant development of hyperlipidemic pancreatitis with severe disease combined with the core features of ferroptosis to explore and describe the mechanism of this phenomenon and shows that the activation of lipid peroxidation and the aberrant intracellular release of many inflammatory mediators during ferroptosis are the key processes that regulate the degree of disease development in patients with HLAP. Inhibiting the activation of ferroptosis effectively reduces the intensity of the inflammatory response, thus reducing organ damage in patients and preventing the risk of HLAP exacerbation. Additionally, this paper summarizes the key targets and potential therapeutic agents of ferroptosis associated with HLAP deterioration to provide new ideas for future clinical applications.

铁死亡的异常激活会加重急性胰腺炎的严重程度，并加剧炎症反应和器官损伤，但详细的潜在机制尚不清楚。与其他类型的胰腺炎相比，高脂血症性急性胰腺炎（HLAP）更容易进展为坏死性胰腺炎，这可能是由于胰周脂肪分解和不饱和脂肪酸的产生所致。此外，高水平的不饱和脂肪酸会发生脂质过氧化并引发铁死亡，进一步加剧炎症并使 HLAP 恶化。本文围绕重症高脂血症性胰腺炎的恶性发展，结合铁死亡的核心特征，探讨和描述该现象的发生机制，表明铁死亡过程中脂质过氧化的激活和细胞内多种炎症介质的异常释放是导致铁死亡的关键因素。调节 HLAP 患者疾病发展程度的关键过程。抑制铁死亡的激活可有效降低炎症反应的强度，从而减轻患者的器官损伤，预防HLAP恶化的风险。此外，本文总结了与HLAP恶化相关的铁死亡的关键靶点和潜在治疗药物，为未来的临床应用提供新思路。