铁死亡在急性胰腺炎中的研究进展

Research progress of ferroptosis in acute pancreatitis

铁死亡是一种铁依赖性的新型细胞程序性死亡方式,已被证明与急性胰腺炎(acute pancreatitis,AP)的发生发展密切相关。通过调控铁离子代谢、活性氧堆积、谷胱甘肽过氧化物酶4以及核转录因子2/血红素氧合酶1与晚期糖基化终产物特异性受体/核转录因子-κB通路的表达,可抑制铁死亡发生,从而预防改善AP。AP是一种常见的消化系统急性病症,10%~20%可发展为重症急性胰腺炎(severe acute pancreatitis,SAP),SAP常合并其他器官(肠黏膜、肝、肺、肾等)损伤。目前,AP尚无明确的发病机制,缺乏有效的治疗方案。本文归纳出铁死亡在AP中的作用机制,及其对SAP引发相关器官(肝、肺、肾、肠黏膜)损伤的影响,以期为疾病的发生机制和预防治疗提供新见解。

Ferroptosis is a new type of iron-dependent programmed cell death,which has been shown to be closely related to the occurrence and development of acute pancreatitis(AP),and can inhibit the occurrence of ferrozois by regulating iron ion metabolism,reactive oxygen species accumulation,glutathione peroxidase 4,and the expression of nuclear transcription factor 2/heme oxygenase 1 and advance glycosylation end-product specific receptor/nuclear transcription factor-kB pathway,thereby preventing and improving AP.AP is a common acute disease of the digestive system.10%~20%of patients can develop into severe acute pancreatitis(SAP).SAP is often associated with damage to other organs(intestinal mucosa,liver,lung,kidney,etc.).At present,there is no clear pathogenesis of AP,and there is no effective treatment plan.In order to provide new insights into the pathogenesis,prevention and treatment of the disease,this review summarizes the mechanism of ferroptosis in AP and its effect on SAP-induced organ damage.