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不同强度机械刺激下颞下颌关节骨关节炎中的关键信号分子

Critical signaling molecules in the temporomandibular joint osteoarthritis under different magnitudes of mechanical stimulation.

作者信息

Liu Yuqi, Jia Fangwen, Li Kangya, Liang Chao, Lin Xiao, Geng Wei, Li Yanxi

机构信息

Department of Dental Implant Center, Beijing Stomatological Hospital, School of Stomatology, Capital Medical University, Beijing, China.

出版信息

Front Pharmacol. 2024 Jul 11;15:1419494. doi: 10.3389/fphar.2024.1419494. eCollection 2024.

DOI:10.3389/fphar.2024.1419494
PMID:39055494
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11269110/
Abstract

The mechanical stress environment in the temporomandibular joint (TMJ) is constantly changing due to daily mandibular movements. Therefore, TMJ tissues, such as condylar cartilage, the synovial membrane and discs, are influenced by different magnitudes of mechanical stimulation. Moderate mechanical stimulation is beneficial for maintaining homeostasis, whereas abnormal mechanical stimulation leads to degeneration and ultimately contributes to the development of temporomandibular joint osteoarthritis (TMJOA), which involves changes in critical signaling molecules. Under abnormal mechanical stimulation, compensatory molecules may prevent degenerative changes while decompensatory molecules aggravate. In this review, we summarize the critical signaling molecules that are stimulated by moderate or abnormal mechanical loading in TMJ tissues, mainly in condylar cartilage. Furthermore, we classify abnormal mechanical stimulation-induced molecules into compensatory or decompensatory molecules. Our aim is to understand the pathophysiological mechanism of TMJ dysfunction more deeply in the ever-changing mechanical environment, and then provide new ideas for discovering effective diagnostic and therapeutic targets in TMJOA.

摘要

由于日常下颌运动,颞下颌关节(TMJ)的机械应力环境不断变化。因此,TMJ组织,如髁突软骨、滑膜和盘,受到不同程度的机械刺激影响。适度的机械刺激有利于维持体内平衡,而异常的机械刺激则导致退变,并最终促使颞下颌关节骨关节炎(TMJOA)的发展,这涉及关键信号分子的变化。在异常机械刺激下,代偿性分子可能预防退变,而失代偿性分子则会加重退变。在这篇综述中,我们总结了TMJ组织(主要是髁突软骨)中由适度或异常机械负荷刺激的关键信号分子。此外,我们将异常机械刺激诱导的分子分为代偿性或失代偿性分子。我们的目的是在不断变化的机械环境中更深入地了解TMJ功能障碍的病理生理机制,进而为发现TMJOA有效的诊断和治疗靶点提供新思路。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b683/11269110/b22dcad76f62/fphar-15-1419494-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b683/11269110/6452c15f8227/fphar-15-1419494-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b683/11269110/8d6540376298/fphar-15-1419494-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b683/11269110/b22dcad76f62/fphar-15-1419494-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b683/11269110/6452c15f8227/fphar-15-1419494-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b683/11269110/8d6540376298/fphar-15-1419494-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b683/11269110/b22dcad76f62/fphar-15-1419494-g003.jpg

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本文引用的文献

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Osteoarthritis Cartilage. 2024 Jun;32(6):666-679. doi: 10.1016/j.joca.2024.02.007. Epub 2024 Feb 23.
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Exploration and breakthrough in the mode of chondrocyte death - A potential new mechanism for osteoarthritis.软骨细胞死亡模式的探索与突破——骨关节炎潜在的新机制
Biomed Pharmacother. 2024 Jan;170:115990. doi: 10.1016/j.biopha.2023.115990. Epub 2023 Dec 6.
3
Abnormal mechanical stress induced chondrocyte senescence by YAP loss-mediated METTL3 upregulation.
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Oral Dis. 2024 Jul;30(5):3308-3320. doi: 10.1111/odi.14810. Epub 2023 Nov 20.
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GSDMD inhibitor protects chondrocyte from mechanical injury in human articular cartilage.GSDMD 抑制剂可保护人关节软骨中的软骨细胞免受机械损伤。
Cell Mol Biol (Noisy-le-grand). 2023 Oct 31;69(10):227-232. doi: 10.14715/cmb/2023.69.10.33.
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Liproxstatin-1 alleviates cartilage degradation by inhibiting chondrocyte ferroptosis in the temporomandibular joint.Liproxstatin-1 通过抑制颞下颌关节软骨细胞铁死亡缓解软骨降解。
Biol Cell. 2024 Jan;116(1):e202300042. doi: 10.1111/boc.202300042. Epub 2023 Nov 9.
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