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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.

DOI:10.2147/JIR.S516502
PMID:40322528
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12050040/
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/aabb00cdbdd7/JIR-18-5867-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ca9/12050040/655d3666ce33/JIR-18-5867-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ca9/12050040/3b6d0f70308f/JIR-18-5867-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ca9/12050040/aabb00cdbdd7/JIR-18-5867-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ca9/12050040/655d3666ce33/JIR-18-5867-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ca9/12050040/3b6d0f70308f/JIR-18-5867-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ca9/12050040/aabb00cdbdd7/JIR-18-5867-g0003.jpg

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本文引用的文献

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Dental Pulp Stem Cells Modulate Inflammasome Pathway and Collagen Deposition of Dermal Fibroblasts.牙髓干细胞调节皮肤成纤维细胞的炎症小体途径和胶原蛋白沉积。
Cells. 2024 May 14;13(10):836. doi: 10.3390/cells13100836.
2
Autophagy induced by hypoxia in pulpitis is mediated by HIF-1α/BNIP3.牙髓炎缺氧诱导的自噬是由 HIF-1α/BNIP3 介导的。
Arch Oral Biol. 2024 Mar;159:105881. doi: 10.1016/j.archoralbio.2024.105881. Epub 2024 Jan 5.
3
Regulated cell death and inflammasome activation in gut injury following traumatic surgery in vitro and in vivo: implication for postoperative death due to multiorgan dysfunction.
体外和体内创伤性手术后肠道损伤中的程序性细胞死亡和炎性小体激活:对多器官功能障碍导致的术后死亡的影响
Cell Death Discov. 2023 Nov 7;9(1):409. doi: 10.1038/s41420-023-01647-z.
4
AR-A014418, a glycogen synthase kinase-3β inhibitor, mitigates lipopolysaccharide-induced inflammation in rat dental pulp stem cells via NLR family pyrin domain containing 3 inflammasome impairment.AR - A014418,一种糖原合酶激酶 - 3β抑制剂,通过损伤含NLR家族pyrin结构域3的炎性小体减轻脂多糖诱导的大鼠牙髓干细胞炎症。
J Dent Sci. 2023 Oct;18(4):1534-1543. doi: 10.1016/j.jds.2023.03.010. Epub 2023 Mar 22.
5
Novel GSDMD inhibitor GI-Y1 protects heart against pyroptosis and ischemia/reperfusion injury by blocking pyroptotic pore formation.新型 GSDMD 抑制剂 GI-Y1 通过阻断细胞焦亡孔形成来保护心脏免受细胞焦亡和缺血/再灌注损伤。
Basic Res Cardiol. 2023 Oct 2;118(1):40. doi: 10.1007/s00395-023-01010-4.
6
Ruxolitinib altered IFN-β induced necroptosis of human dental pulp stem cells during osteoblast differentiation.鲁索替尼在成骨细胞分化过程中改变了干扰素-β诱导的人牙髓干细胞坏死性凋亡。
Arch Oral Biol. 2023 Nov;155:105797. doi: 10.1016/j.archoralbio.2023.105797. Epub 2023 Aug 22.
7
Synoviolin alleviates GSDMD-mediated periodontitis by suppressing its stability.滑膜凝蛋白通过抑制 GSDMD 的稳定性来缓解 GSDMD 介导的牙周炎。
Immun Inflamm Dis. 2023 Jul;11(7):e880. doi: 10.1002/iid3.880.
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Palmitic acid induces GSDMD-mediated pyroptosis in periodontal ligament cells via the NF-κB pathway.软脂酸通过 NF-κB 通路诱导牙周膜细胞中 GSDMD 介导的细胞焦亡。
Oral Dis. 2024 May;30(4):2546-2557. doi: 10.1111/odi.14648. Epub 2023 Jun 25.
9
The effects of dimethyl fumarate on cytoplasmic LPS-induced noncanonical pyroptosis in periodontal ligament fibroblasts and dental pulp cells.富马酸二甲酯对牙周膜成纤维细胞和牙髓细胞中细胞质 LPS 诱导的非典型细胞焦亡的影响。
Int Endod J. 2023 Jul;56(7):869-880. doi: 10.1111/iej.13926. Epub 2023 May 6.
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Piceatannol protects against age-related hearing loss by inhibiting cellular pyroptosis and inflammation through regulated Caspase11-GSDMD pathway.白皮杉醇通过调控 Caspase11-GSDMD 通路抑制细胞焦亡和炎症反应来防治与年龄相关的听力损失。
Biomed Pharmacother. 2023 Jul;163:114704. doi: 10.1016/j.biopha.2023.114704. Epub 2023 Apr 24.