细胞衰老:抑制牙周炎的新视角(综述)。

IF 3.4 3区 医学 Q2 MEDICINE, RESEARCH & EXPERIMENTAL Molecular medicine reports Pub Date : 2024-12-01 Epub Date: 2024-10-18 DOI:10.3892/mmr.2024.13362
Xue-Jing Lin, Qing Yuan, Jie Zhou, Yu-Lei Dong, Diwas Sunchuri, Zhu-Ling Guo
{"title":"细胞衰老:抑制牙周炎的新视角(综述)。","authors":"Xue-Jing Lin, Qing Yuan, Jie Zhou, Yu-Lei Dong, Diwas Sunchuri, Zhu-Ling Guo","doi":"10.3892/mmr.2024.13362","DOIUrl":null,"url":null,"abstract":"<p><p>Cellular senescence, characterized by cell cycle arrest, can result in tissue dysfunction when senescent cells persist and accumulate. Periodontitis, a chronic inflammatory condition caused by the interaction between bacteria and the immune system of the host, primarily manifests as damage to periodontal tissues. Aging and inflammation are interlinked processes that exacerbate each other. The progression of localized chronic periodontal inflammation is often accelerated in conjunction with tissue and organ aging. The presence of senescent cells and release of inflammatory cytokines, immune modulators, growth factors and proteases that are associated with the senescence‑associated secretory phenotype contribute to the deterioration of periodontal tissues. The present review aimed to elucidate the mechanisms of cellular senescence and its potential impact on periodontitis, offering novel insights for modulating the inflammatory microenvironment of periodontal tissues.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"30 6","pages":""},"PeriodicalIF":3.4000,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11529191/pdf/","citationCount":"0","resultStr":"{\"title\":\"Cellular senescence: A new perspective on the suppression of periodontitis (Review).\",\"authors\":\"Xue-Jing Lin, Qing Yuan, Jie Zhou, Yu-Lei Dong, Diwas Sunchuri, Zhu-Ling Guo\",\"doi\":\"10.3892/mmr.2024.13362\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Cellular senescence, characterized by cell cycle arrest, can result in tissue dysfunction when senescent cells persist and accumulate. Periodontitis, a chronic inflammatory condition caused by the interaction between bacteria and the immune system of the host, primarily manifests as damage to periodontal tissues. Aging and inflammation are interlinked processes that exacerbate each other. The progression of localized chronic periodontal inflammation is often accelerated in conjunction with tissue and organ aging. The presence of senescent cells and release of inflammatory cytokines, immune modulators, growth factors and proteases that are associated with the senescence‑associated secretory phenotype contribute to the deterioration of periodontal tissues. The present review aimed to elucidate the mechanisms of cellular senescence and its potential impact on periodontitis, offering novel insights for modulating the inflammatory microenvironment of periodontal tissues.</p>\",\"PeriodicalId\":18818,\"journal\":{\"name\":\"Molecular medicine reports\",\"volume\":\"30 6\",\"pages\":\"\"},\"PeriodicalIF\":3.4000,\"publicationDate\":\"2024-12-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11529191/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Molecular medicine reports\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.3892/mmr.2024.13362\",\"RegionNum\":3,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2024/10/18 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q2\",\"JCRName\":\"MEDICINE, RESEARCH & EXPERIMENTAL\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Molecular medicine reports","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.3892/mmr.2024.13362","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/10/18 0:00:00","PubModel":"Epub","JCR":"Q2","JCRName":"MEDICINE, RESEARCH & EXPERIMENTAL","Score":null,"Total":0}
引用次数: 0

摘要

细胞衰老的特点是细胞周期停滞,当衰老细胞持续积累时,会导致组织功能障碍。牙周炎是一种慢性炎症,由细菌和宿主免疫系统相互作用引起,主要表现为牙周组织受损。衰老和炎症是相互关联的过程,会相互加重。局部慢性牙周炎症的进展往往会随着组织和器官的衰老而加速。衰老细胞的存在以及与衰老相关分泌表型有关的炎性细胞因子、免疫调节剂、生长因子和蛋白酶的释放,都会导致牙周组织的恶化。本综述旨在阐明细胞衰老的机制及其对牙周炎的潜在影响,为调节牙周组织的炎症微环境提供新的见解。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
Cellular senescence: A new perspective on the suppression of periodontitis (Review).

Cellular senescence, characterized by cell cycle arrest, can result in tissue dysfunction when senescent cells persist and accumulate. Periodontitis, a chronic inflammatory condition caused by the interaction between bacteria and the immune system of the host, primarily manifests as damage to periodontal tissues. Aging and inflammation are interlinked processes that exacerbate each other. The progression of localized chronic periodontal inflammation is often accelerated in conjunction with tissue and organ aging. The presence of senescent cells and release of inflammatory cytokines, immune modulators, growth factors and proteases that are associated with the senescence‑associated secretory phenotype contribute to the deterioration of periodontal tissues. The present review aimed to elucidate the mechanisms of cellular senescence and its potential impact on periodontitis, offering novel insights for modulating the inflammatory microenvironment of periodontal tissues.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
Molecular medicine reports
Molecular medicine reports 医学-病理学
CiteScore
7.60
自引率
0.00%
发文量
321
审稿时长
1.5 months
期刊介绍: Molecular Medicine Reports is a monthly, peer-reviewed journal available in print and online, that includes studies devoted to molecular medicine, underscoring aspects including pharmacology, pathology, genetics, neurosciences, infectious diseases, molecular cardiology and molecular surgery. In vitro and in vivo studies of experimental model systems pertaining to the mechanisms of a variety of diseases offer researchers the necessary tools and knowledge with which to aid the diagnosis and treatment of human diseases.
期刊最新文献
Solamargine inhibits gastric cancer progression via inactivation of STAT3/PD‑L1 signaling. [Retracted] lncRNA DQ786243 promotes hepatocellular carcinoma cell invasion and proliferation by regulating the miR‑15b‑5p/Wnt3A axis. Ophiopogon japonicus polysaccharide reduces doxorubicin-induced myocardial ferroptosis injury by activating Nrf2/GPX4 signaling and alleviating iron accumulation. Ciliary neurotrophic factor activation of astrocytes mediates neuronal damage via the IL‑6/IL‑6R pathway. MDM2 interacts with PTEN to inhibit endothelial cell development and promote deep vein thrombosis via the JAK/STAT signaling pathway.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1