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衰老细胞:骨质疏松症的一个治疗靶点。

Senescent cells: A therapeutic target for osteoporosis.

作者信息

Wang Tiantian, Huang Shishu, He Chengqi

机构信息

Department of Rehabilitation Medicine, Key Laboratory of Rehabilitation Medicine, West China Hospital, Sichuan University, Chengdu, Sichuan, China.

Institute of Rehabilitation Medicine, West China Hospital, Sichuan University, Chengdu, Sichuan, China.

出版信息

Cell Prolif. 2022 Dec;55(12):e13323. doi: 10.1111/cpr.13323. Epub 2022 Aug 19.


DOI:10.1111/cpr.13323
PMID:35986568
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9715365/
Abstract

BACKGROUND: Osteoporosis (OP) is a prevalent disorder characterized by the loss of bone mass and the deterioration of bone microarchitecture. OP is attributed to various factors, including menopause (primary), ageing (primary) and the adverse effects of medications (secondary). Recently, cellular senescence has been shown to have a crucial role in the maintenance of cellular homeostasis and organ function. The purpose of this review is to summarize recent findings regarding the roles of bone cellular senescence and senescence-associated secretory phenotype (SASP) in OP. METHODS: A comprehensive search of the PubMed database from inception to July 2022 was performed regarding the molecular mechanism of bone cell senescence in OP progression. RESULTS: We describe the pathophysiology of senescent bone cells and SASP, and how each contributes to OP. We also provide new options for treating OP by targeting cellular senescence pathways. CONCLUSION: Cellular senescence plays an important role in bone homeostasis, with variations based on the different types of OP. These variations are associated with pathogenic factors, bone turnover rate and systemic metabolism. Understanding the molecular relationship between bone cells and senescence provides for the possible targeting of senescence as a means by which to treat OP.

摘要

背景:骨质疏松症(OP)是一种常见疾病,其特征为骨量丢失和骨微结构恶化。OP 归因于多种因素,包括绝经(原发性)、衰老(原发性)以及药物的不良反应(继发性)。最近研究表明,细胞衰老在维持细胞稳态和器官功能方面起着关键作用。本综述的目的是总结关于骨细胞衰老和衰老相关分泌表型(SASP)在 OP 中作用的最新研究结果。 方法:对 PubMed 数据库从建库至 2022 年 7 月进行全面检索,以获取有关 OP 进展中骨细胞衰老分子机制的相关信息。 结果:我们阐述了衰老骨细胞和 SASP 的病理生理学,以及它们各自如何导致 OP。我们还通过靶向细胞衰老途径为治疗 OP 提供了新的选择。 结论:细胞衰老在骨稳态中起重要作用,根据不同类型的 OP 存在差异。这些差异与致病因素、骨转换率和全身代谢有关。了解骨细胞与衰老之间的分子关系为将衰老作为治疗 OP 的一种手段提供了可能的靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a246/9715365/784f66475ffe/CPR-55-e13323-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a246/9715365/1cc4b46353a3/CPR-55-e13323-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a246/9715365/aab11542a99e/CPR-55-e13323-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a246/9715365/0eebe0296673/CPR-55-e13323-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a246/9715365/784f66475ffe/CPR-55-e13323-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a246/9715365/1cc4b46353a3/CPR-55-e13323-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a246/9715365/aab11542a99e/CPR-55-e13323-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a246/9715365/0eebe0296673/CPR-55-e13323-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a246/9715365/784f66475ffe/CPR-55-e13323-g002.jpg

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[6]
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[7]
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[8]
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[9]
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[10]
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本文引用的文献

[1]
Pulsed electromagnetic fields attenuate glucocorticoid-induced bone loss by targeting senescent LepR bone marrow mesenchymal stromal cells.

Biomater Adv. 2022-2

[2]
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Ageing Res Rev. 2022-5

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Ageing Res Rev. 2022-5

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Pharmacol Ther. 2022-9

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J Clin Invest. 2022-2-1

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An antibody against Siglec-15 promotes bone formation and fracture healing by increasing TRAP mononuclear cells and PDGF-BB secretion.

Bone Res. 2021-11-1

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FEBS J. 2022-3

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Senescent immune cells release grancalcin to promote skeletal aging.

Cell Metab. 2021-10-5

[9]
Extracellular vesicles from adipose tissue-derived stem cells alleviate osteoporosis through osteoprotegerin and miR-21-5p.

J Extracell Vesicles. 2021-10

[10]
Cellular senescence in musculoskeletal homeostasis, diseases, and regeneration.

Bone Res. 2021-9-10

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