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牙髓炎中的细胞焦亡

Pyroptosis in Pulpitis.

作者信息

Wei Xiaorui, Ran Shidian, Yan Xingrui, Huang Jindie, Xue Linyu, He Tong-Chuan, Zhang Hongmei, Wu Si

机构信息

The Affiliated Stomatological Hospital of Chongqing Medical University, Chongqing Key Laboratory of Oral Diseases, Chongqing Municipal Key Laboratory of Oral Biomedical Engineering of Higher Education, Chongqing Municipal Health Commission Key Laboratory of Oral Biomedical Engineering, Chongqing, People's Republic of China.

Molecular Oncology Laboratory, Department of Orthopaedic Surgery and Rehabilitation Medicine, The University of Chicago Medical Center, Chicago, IL, USA.

出版信息

J Inflamm Res. 2025 Apr 30;18:5867-5879. doi: 10.2147/JIR.S516502. eCollection 2025.

Abstract

Pulpitis is an inflammatory disease occurs in the pulp tissues. Continuous development of pulpitis can lead to apical periodontitis and seriously damage the function of teeth, affecting the oral health and daily life of patients. Pyroptosis, alternatively termed inflammatory necrosis, is a type of programmed cell death that is characterized by the swelling of cells until the cell membrane is broken. The GSDM family of proteins can be activated by a variety of pathways, which can lead to the puncture of cell membrane, inducing the release of cellular contents and inflammatory cytokines like IL-1β and IL-18 to activate a strong inflammatory response. Pyroptosis in dental pulp may be an important direction to find new targets for pulpal inflammation prevention and treatment, which deserves further study. In this article, we reviewed the activation mechanism and potential role of pyroptosis in the progression of pulpitis, along with the interaction between pyroptosis and other regulated cell death (RCD) pathways. This review aims to enrich the mechanism under the development of dental pulp inflammation, and to uncover potential therapeutic targets for early alleviation and treatment of pulp inflammation.

摘要

牙髓炎是发生在牙髓组织的一种炎症性疾病。牙髓炎的持续发展可导致根尖周炎,并严重损害牙齿功能,影响患者的口腔健康和日常生活。细胞焦亡,又称炎性坏死,是一种程序性细胞死亡,其特征是细胞肿胀直至细胞膜破裂。GSDM蛋白家族可通过多种途径被激活,这会导致细胞膜穿孔,诱导细胞内容物和炎性细胞因子如IL-1β和IL-18的释放,从而激活强烈的炎症反应。牙髓中的细胞焦亡可能是寻找预防和治疗牙髓炎症新靶点的一个重要方向,值得进一步研究。在本文中,我们综述了细胞焦亡在牙髓炎进展中的激活机制和潜在作用,以及细胞焦亡与其他调节性细胞死亡(RCD)途径之间的相互作用。本综述旨在丰富牙髓炎症发生发展的机制,并揭示早期缓解和治疗牙髓炎症的潜在治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ca9/12050040/655d3666ce33/JIR-18-5867-g0001.jpg

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