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细胞衰老:抑制牙周炎的新视角(综述)。

Cellular senescence: A new perspective on the suppression of periodontitis (Review).

机构信息

School of Dentistry, Hainan Medical University, Haikou, Hainan 571199, P.R. China.

School of International Education, Hainan Medical University, Haikou, Hainan 571199, P.R. China.

出版信息

Mol Med Rep. 2024 Dec;30(6). doi: 10.3892/mmr.2024.13362. Epub 2024 Oct 18.


DOI:10.3892/mmr.2024.13362
PMID:39422030
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11529191/
Abstract

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.

摘要

细胞衰老的特征是细胞周期停滞,如果衰老细胞持续积累,可能导致组织功能障碍。牙周炎是一种由细菌与宿主免疫系统相互作用引起的慢性炎症性疾病,主要表现为牙周组织损伤。衰老和炎症是相互关联的过程,会相互加剧。局部慢性牙周炎的进展常与组织和器官衰老同时加速。衰老细胞的存在和与衰老相关分泌表型相关的炎症细胞因子、免疫调节剂、生长因子和蛋白酶的释放,导致牙周组织恶化。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。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d2de/11529191/b3557603b853/mmr-30-06-13362-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d2de/11529191/b97cbf833b35/mmr-30-06-13362-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d2de/11529191/b3557603b853/mmr-30-06-13362-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d2de/11529191/b97cbf833b35/mmr-30-06-13362-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d2de/11529191/b3557603b853/mmr-30-06-13362-g01.jpg

相似文献

[1]
Cellular senescence: A new perspective on the suppression of periodontitis (Review).

Mol Med Rep. 2024-12

[2]
Cellular senescence with SASP in periodontal ligament cells triggers inflammation in aging periodontal tissue.

Aging (Albany NY). 2023-3-1

[3]
The Emerging Role of Accelerated Cellular Senescence in Periodontitis.

J Dent Res. 2023-7

[4]
Molecular Signatures of Senescence in Periodontitis: Clinical Insights.

J Dent Res. 2024-7

[5]
Cellular Senescence and Periodontitis: Mechanisms and Therapeutics.

Biology (Basel). 2022-9-29

[6]
Senescent cells exacerbate chronic inflammation and contribute to periodontal disease progression in old mice.

J Periodontol. 2021-10

[7]
Mechanisms and Regulation of Cellular Senescence.

Int J Mol Sci. 2021-12-6

[8]
Cellular senescence in the lung across the age spectrum.

Am J Physiol Lung Cell Mol Physiol. 2019-2-20

[9]
Senescent cells as a source of inflammatory factors for tumor progression.

Cancer Metastasis Rev. 2010-6

[10]
Periodontal Disease and Senescent Cells: New Players for an Old Oral Health Problem?

Int J Mol Sci. 2020-10-9

引用本文的文献

[1]
Nutritional intake and health status of populations and the relationship between diet and oral ulcers: A cross-sectional study based on NHANES data and machine learning predictions.

Medicine (Baltimore). 2025-7-18

本文引用的文献

[1]
Oxygen, the Paradox of Life and the Eye.

Front Biosci (Landmark Ed). 2024-9-13

[2]
The role of p21 in cellular senescence and aging-related diseases.

Mol Cells. 2024-11

[3]
METTL14-mediated HOXA5 mA modification alleviates osteoporosis via promoting WNK1 transcription to suppress NLRP3-dependent macrophage pyroptosis.

J Orthop Translat. 2024-8-27

[4]
IL-10 deficiency aggravates cell senescence and accelerates BLM-induced pulmonary fibrosis in aged mice via PTEN/AKT/ERK pathway.

BMC Pulm Med. 2024-9-11

[5]
Cellular senescence and SASP in tumor progression and therapeutic opportunities.

Mol Cancer. 2024-8-31

[6]
The role of deacetylase SIRT1 in allergic diseases.

Front Immunol. 2024

[7]
Autophagy regulates age-related delayed jawbone regeneration and decreased osteoblast osteogenesis by degrading FABP3.

FASEB J. 2024-7-31

[8]
Strategies for modeling aging and age-related diseases.

NPJ Aging. 2024-7-10

[9]
Neutrophils and neutrophil extracellular traps in oral health and disease.

Exp Mol Med. 2024-5

[10]
Prevalence of Periodontal Disease among Patients Reporting to Tertiary Care Hospital in Ranchi.

J Pharm Bioallied Sci. 2024-2

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