Pyroptosis of chondrocytes activated by synovial inflammation accelerates TMJ osteoarthritis cartilage degeneration via ROS/NLRP3 signaling

上睑下垂 软骨细胞 软骨 滑膜炎 炎症 骨关节炎 医学 滑膜关节 滑液 免疫学 病理 炎症体 关节炎 解剖 关节软骨 替代医学
作者
Xin Liu,Yanyan Li,Jie Zhao,Zhihui Hu,Wei Fang,Ke Jin,Wei Li,Xing Long
出处
期刊:International Immunopharmacology [Elsevier]
卷期号:124: 110781-110781 被引量:5
标识
DOI:10.1016/j.intimp.2023.110781
摘要

Synovial inflammation and chondrocyte death have been widely acknowledged as key contributors to the pathological progression of temporomandibular joint osteoarthritis (TMJ-OA), a degenerative joint disease currently lacking definitive treatments. This study aims to understand the regulatory role of chondrocyte pyroptosis in condylar cartilage degradation during TMJ-OA.The levels of cytokines, cartilage degeneration markers, and pyroptotic biomarkers in the synovium and synovial fluid of temporomandibular disorders (TMD) patients were examined. The synovitis, cartilage degradation, and chondrocyte pyroptosis in wild-type and alpha-kinase 1 (ALPK1)-deficient TMJ-OA mice were then compared following monosodium iodoacetate (MIA) induction. Subsequently, we investigated the downstream mechanisms of cytokines- or macrophage supernatants-induced metabolic disorders and pyroptosis in chondrocytes using primary TMJ chondrocytes and ATDC5 chondrocyte cultures.We found a positive correlation between pyroptotic biomarkers and cartilage degradation mediators and cytokines in the synovial fluid of TMD patients. MIA-induced TMJ-OA mice demonstrated significant synovitis, cartilage degradation, and chondrocyte pyroptosis, which were mitigated in ALPK1-deficient TMJ-OA mice, inflammation-restrained mice. Ex-vivo study revealed the contribution of reactive oxygen species (ROS) to inflammation-irritated macrophage supernatants-induced pyroptosis and metabolic disorders in chondrocytes. Targeting NOD-like receptor protein 3 (NLRP3) alleviated cytokines- or ROS-induced pyroptosis and metabolic disorders in chondrocytes by inhibiting caspase-1 activation and interleukin-1β (IL-1β) secretion.Our findings offer novel insight into the role of synovial inflammation-induced chondrocyte pyroptosis in promoting cartilage degradation during TMJ-OA via the ROS and NLRP3 signaling pathway.
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
大幅提高文件上传限制,最高150M (2024-4-1)

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
Akim应助LJJZZX采纳,获得10
刚刚
小凡完成签到 ,获得积分20
刚刚
善学以致用应助小明采纳,获得10
刚刚
1秒前
刘晶发布了新的文献求助10
3秒前
科研通AI2S应助Dsivan采纳,获得10
3秒前
LXOYL应助zero采纳,获得10
4秒前
时尚凡雁发布了新的文献求助10
4秒前
可爱的函函应助格格星采纳,获得10
5秒前
6秒前
赘婿应助明理的喵采纳,获得10
7秒前
8秒前
小乐儿~完成签到,获得积分10
9秒前
9秒前
10秒前
如沐风完成签到,获得积分20
10秒前
Dsivan完成签到,获得积分10
11秒前
圆圆完成签到 ,获得积分10
11秒前
今后应助LOMO采纳,获得30
12秒前
12秒前
如沐风发布了新的文献求助10
13秒前
积极睫毛完成签到,获得积分10
14秒前
万能图书馆应助7尔阿婆采纳,获得10
14秒前
Hodge完成签到,获得积分10
14秒前
白樱恋曲发布了新的文献求助10
15秒前
15秒前
完美世界应助火速阿百川采纳,获得10
16秒前
16秒前
酷波er应助Renzhiihao采纳,获得30
17秒前
哭泣的灵煌完成签到,获得积分10
19秒前
嘉嘉Joey完成签到 ,获得积分10
20秒前
优雅沛文发布了新的文献求助10
20秒前
20秒前
21秒前
zjkzh完成签到,获得积分10
22秒前
嘉嘉Joey关注了科研通微信公众号
23秒前
23秒前
复杂雨双发布了新的文献求助10
25秒前
stuffmatter应助Singularity采纳,获得10
25秒前
26秒前
高分求助中
中国国际图书贸易总公司40周年纪念文集 大事记1949-1987 2000
TM 5-855-1(Fundamentals of protective design for conventional weapons) 1000
草地生态学 880
Threaded Harmony: A Sustainable Approach to Fashion 799
Basic Modern Theory of Linear Complex Analytic 𝑞-Difference Equations 500
Queer Politics in Times of New Authoritarianisms: Popular Culture in South Asia 500
Livre et militantisme : La Cité éditeur 1958-1967 500
热门求助领域 (近24小时)
化学 医学 生物 材料科学 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 基因 遗传学 催化作用 物理化学 免疫学 量子力学 细胞生物学
热门帖子
关注 科研通微信公众号,转发送积分 3058290
求助须知:如何正确求助?哪些是违规求助? 2714427
关于积分的说明 7440509
捐赠科研通 2359692
什么是DOI,文献DOI怎么找? 1250302
科研通“疑难数据库(出版商)”最低求助积分说明 607401
版权声明 596410