骨性关节炎中细胞焦亡的影响及其机制OA
The Impact and Mechanism of Cell Pyroptosis in Osteoarthritis
近年来的研究揭示了除凋亡与坏死之外,由极端微环境因素诱导的新的细胞死亡形式.细胞焦亡是一种受调控的细胞死亡形式,当模式识别受体识别相关配体并激活半胱氨酸天冬氨酸蛋白酶1(Caspase-1)或Caspase-11时发生,进而触发促炎细胞因子白细胞介素-1β(IL-1β)和白细胞介素-18(IL-18)的成熟与释放.骨关节炎(Osteoarthri-tis,OA)作为全球最常见的关节疾病,以轻度炎症和包括IL-1 β、IL-18在内的促炎细胞因子水平升高为主要临床特征.此外,在OA发病过程中,部分受损软骨细胞表现出与焦亡相似的形态学特征.焦亡作为一种调控性细胞死亡,可参与骨关节炎的病理生理过程.该文综述了细胞焦亡的分子机制,并重点阐述NLRP3炎性小体(NLR家族,pyrin结构域包含蛋白3)在其中的作用.本研究旨在阐明细胞焦亡在OA发病机制中的作用,以期为OA的防治提供新的思路.
Recent studies have revealed novel forms of cell death,distinct from apoptosis and necrosis,that are induced by extreme microenvironmental factors.Pyroptosis is a regulated form of cell death that occurs when pattern recognition receptors(PRRs)induce the activation of caspase-1 or caspase-11,leading to the maturation and release of the proinflammatory cyto-kines IL-1 βand IL-1 8.Osteoarthritis(OA),the most prevalent joint disease worldwide,is characterized by mild inflamma-tion and elevated cytokine levels,including IL-1βand IL-18.Moreover,some damaged chondrocytes exhibit morphological alterations resembling pyroptosis during OA pathogenesis.This regulatory cell death process can contribute to the pathological al-terations observed in OA.This review summarizes the molecular mechanisms underlying pyroptosis and the role of the NLRP3 in-flammasome(NLR family,pyrin domain containing 3)in this process.This review aims to elucidate the role of pyroptosis in the pathogenesis of OA,highlighting its potential significance.
黄琰;张宇;郑曲;陈巍;宫云昭
辽宁中医药大学第二临床学院,辽宁 沈阳 110034辽宁中医药大学,辽宁 沈阳 110847辽宁中医药大学,辽宁 沈阳 110847辽宁中医药大学第二临床学院,辽宁 沈阳 110034辽宁中医药大学第二临床学院,辽宁 沈阳 110034||辽宁中医药大学,辽宁 沈阳 110847
医药卫生
骨关节炎细胞焦亡NLRP3
OsteoarthritisPyroptosisNLRP3 inflammasome
《实用中医内科杂志》 2026 (4)
113-117,后插28,6
辽宁省科技计划联合计划(基金)项目(2023-MSLH-143)辽宁省教育厅高校基本科研项目(面上项目)(LJKMZ20221327)
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