Aging and the emerging role of cellular senescence in osteoarthritis

衰老 细胞衰老 骨关节炎 医学 生物 老年学 物理医学与康复 病理 遗传学 内科学 基因 表型 替代医学
作者
Brian O. Diekman,Richard F. Loeser
出处
期刊:Osteoarthritis and Cartilage [Elsevier BV]
卷期号:32 (4): 365-371 被引量:19
标识
DOI:10.1016/j.joca.2023.11.018
摘要

Summary

Objective

The correlation between age and incidence of osteoarthritis (OA) is well known but the causal mechanisms involved are not completely understood. This narrative review summarizes selected key findings from the past 30 years that have elucidated key aspects of the relationship between aging and OA.

Methods

The peer-reviewed English language literature was searched on PubMed using keywords including senescence, aging, cartilage, and osteoarthritis, for original studies and reviews published from 1993 to 2023 with a major focus on more recent studies. Manuscripts most relevant to aging and OA that examined one or more of the hallmarks of aging were selected for further review.

Results

All proposed hallmarks of aging have been observed in articular cartilage and some have also been described in other joint tissues. Hallmarks include genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, deregulated nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, altered intercellular communication, disabled macroautophagy, chronic inflammation, and dysbiosis. There is evidence that these age-related changes contribute to the development of OA in part by promoting cellular senescence. Senescence may therefore serve as a downstream mediator that connects numerous aging hallmarks to OA, likely through the senescence-associated secretory phenotype that is characterized by increased production of proinflammatory cytokines and matrix metalloproteinases.

Conclusions

Progress over the past 30 years has provided the foundation for emerging therapies, such as senolytics and senomorphics, that hold promise for OA disease modification. Mechanistic studies utilizing physiologically-aged animals and cadaveric human joint tissues will be important for continued progress.
最长约 10秒,即可获得该文献文件

科研通智能强力驱动
Strongly Powered by AbleSci AI
更新
PDF的下载单位、IP信息已删除 (2025-6-4)

科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
1秒前
1秒前
爱吃萝卜的Bob完成签到,获得积分10
2秒前
啵妞完成签到 ,获得积分10
2秒前
hulibin1208完成签到,获得积分10
2秒前
郁香薇发布了新的文献求助10
3秒前
hehe完成签到,获得积分10
3秒前
IrisFang1030完成签到,获得积分10
3秒前
3秒前
开心人达发布了新的文献求助10
4秒前
HPP123发布了新的文献求助10
4秒前
无情白羊发布了新的文献求助10
5秒前
6秒前
6秒前
dong应助ayuelei采纳,获得10
6秒前
Espionage发布了新的文献求助10
7秒前
7秒前
mmm发布了新的文献求助30
8秒前
上官又莲完成签到,获得积分10
8秒前
量子星尘发布了新的文献求助30
8秒前
Dana完成签到,获得积分10
8秒前
9秒前
英姑应助fafa采纳,获得10
10秒前
朝气发布了新的文献求助10
10秒前
烟花应助斤斤采纳,获得10
10秒前
hehe发布了新的文献求助10
12秒前
12秒前
隐形曼青应助what采纳,获得10
12秒前
asdfghjkl完成签到,获得积分10
13秒前
yanguowusheng完成签到 ,获得积分10
14秒前
jianlong0206完成签到,获得积分10
14秒前
痕丶歆完成签到 ,获得积分10
14秒前
15秒前
15秒前
XHH1994发布了新的文献求助10
15秒前
斯文败类应助NCS采纳,获得10
15秒前
wangayting完成签到,获得积分10
15秒前
15秒前
17秒前
suolonglong完成签到,获得积分10
17秒前
高分求助中
A new approach to the extrapolation of accelerated life test data 1000
Cognitive Neuroscience: The Biology of the Mind 1000
Technical Brochure TB 814: LPIT applications in HV gas insulated switchgear 1000
ACSM’s Guidelines for Exercise Testing and Prescription, 12th edition 500
Picture Books with Same-sex Parented Families: Unintentional Censorship 500
Nucleophilic substitution in azasydnone-modified dinitroanisoles 500
不知道标题是什么 500
热门求助领域 (近24小时)
化学 材料科学 医学 生物 工程类 有机化学 生物化学 物理 内科学 纳米技术 计算机科学 化学工程 复合材料 遗传学 基因 物理化学 催化作用 冶金 细胞生物学 免疫学
热门帖子
关注 科研通微信公众号,转发送积分 3969513
求助须知:如何正确求助?哪些是违规求助? 3514327
关于积分的说明 11173617
捐赠科研通 3249672
什么是DOI,文献DOI怎么找? 1794973
邀请新用户注册赠送积分活动 875537
科研通“疑难数据库(出版商)”最低求助积分说明 804836