细胞焦亡在腹膜纤维化发生、发展中作用的研究进展  被引量:1

Research progress on the role of pyroptosis in the occurrence and development of peritoneal fibrosis

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作  者:薛丹丹 李相[1] 马小芬[1] 焦占峰[1] 张宜明[1] Xue Dandan;Li Xiang;Ma Xiaofen;Jiao Zhanfeng;Zhang Yiming(Department of Nephrology,Affiliated Hospital of Jining Medical College,Jining 272029,China)

机构地区:[1]济宁医学院附属医院肾内科,济宁272029

出  处:《中国医师杂志》2023年第6期958-960,F0003,共4页Journal of Chinese Physician

基  金:山东省中医药科技发展计划项目(2019-0484)。

摘  要:腹膜透析是一种公认的肾脏替代疗法。长期腹膜透析会导致腹膜的形态和功能改变,即腹膜纤维化,是导致腹膜超滤能力丧失的已知原因。细胞焦亡是一种特殊类型的溶血性程序性细胞死亡,以细胞肿胀、破裂、分泌细胞内容物和显著的促炎症作用为特征。细胞焦亡可分为典型途径和非典型途径,其中NOD样受体热蛋白结构域相关蛋白3(NLRP3)炎性小体是最重要的引发剂。目前的证据表明,高糖腹膜透析液可诱导腹膜间皮细胞焦亡,其引起的炎症和细胞损伤可加重腹膜纤维化进展,不同的信号通路已被证明可调节细胞焦亡的发生。最新的研究证明一些潜在的靶向抑制焦亡的方法,可有效抑制腹膜间皮细胞炎症并缓解腹膜纤维化。该文章主要对细胞焦亡的分子机制及细胞焦亡与腹膜纤维化的关系进行论述。Peritoneal dialysis is a recognized renal replacement therapy.Long term peritoneal dialysis will lead to changes in the morphology and function of the peritoneum,that is,peritoneal fibrosis,which is a known cause of the loss of peritoneal ultrafiltration capacity.Pyroptosis is a special type of soluble programmed cell death,characterized by cell swelling,rupture,secretion of cell contents and significant proinflammatory effect.The pyroptosis can be divided into typical and atypical pathways,and the inflammatory body of NOD like receptor heat protein domain related protein 3(NLRP3)is the most important initiator.Current evidence shows that high glucose peritoneal dialysis fluid can induce peritoneal Mesothelium to scorch,and the inflammation and cell damage caused by it can aggravate the progress of peritoneal fibrosis.Different signal pathways have been proved to regulate the occurrence of pyroptosis.The latest research has proved that some potential targeted methods to inhibit pyroptosis can effectively inhibit the inflammation of peritoneal mesothelium and alleviate peritoneal fibrosis.This article mainly discusses the molecular mechanism of pyroptosis and the relationship between pyroptosis and peritoneal fibrosis.

关 键 词:细胞焦亡 腹膜透析 腹膜纤维化 

分 类 号:R572.2[医药卫生—消化系统]

 

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