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健康关节和骨关节炎关节面临的细胞串扰。

Healthy and Osteoarthritis-Affected Joints Facing the Cellular Crosstalk.

机构信息

Department of Doctoral Studies, Rīga Stradiņš University, LV-1007 Riga, Latvia.

Joint Laboratory of Electron Microscopy, Institute of Anatomy and Anthropology, Rīga Stradiņš University, LV-1007 Riga, Latvia.

出版信息

Int J Mol Sci. 2023 Feb 18;24(4):4120. doi: 10.3390/ijms24044120.

DOI:10.3390/ijms24044120
PMID:36835530
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9964755/
Abstract

Osteoarthritis (OA) is a chronic, progressive, severely debilitating, and multifactorial joint disease that is recognized as the most common type of arthritis. During the last decade, it shows an incremental global rise in prevalence and incidence. The interaction between etiologic factors that mediate joint degradation has been explored in numerous studies. However, the underlying processes that induce OA remain obscure, largely due to the variety and complexity of these mechanisms. During synovial joint dysfunction, the osteochondral unit undergoes cellular phenotypic and functional alterations. At the cellular level, the synovial membrane is influenced by cartilage and subchondral bone cleavage fragments and extracellular matrix (ECM) degradation products from apoptotic and necrotic cells. These "foreign bodies" serve as danger-associated molecular patterns (DAMPs) that trigger innate immunity, eliciting and sustaining low-grade inflammation in the synovium. In this review, we explore the cellular and molecular communication networks established between the major joint compartments-the synovial membrane, cartilage, and subchondral bone of normal and OA-affected joints.

摘要

骨关节炎(OA)是一种慢性、进行性、严重致残和多因素的关节疾病,被认为是最常见的关节炎类型。在过去十年中,它的患病率和发病率呈全球性递增趋势。许多研究都探讨了介导关节降解的病因因素之间的相互作用。然而,导致 OA 的潜在过程仍然不清楚,这主要是由于这些机制的多样性和复杂性。在滑液关节功能障碍期间,软骨下骨单元经历细胞表型和功能的改变。在细胞水平上,滑膜受软骨和软骨下骨裂解片段以及来自凋亡和坏死细胞的细胞外基质(ECM)降解产物的影响。这些“异物”作为危险相关分子模式(DAMPs),触发先天免疫,在滑膜中引发和维持低度炎症。在这篇综述中,我们探讨了正常关节和 OA 关节的主要关节间隙——滑膜、软骨和软骨下骨之间建立的细胞和分子通讯网络。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0747/9964755/8d79a5a6ed24/ijms-24-04120-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0747/9964755/e1c52bc8278f/ijms-24-04120-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0747/9964755/8041b46bb7e8/ijms-24-04120-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0747/9964755/8d79a5a6ed24/ijms-24-04120-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0747/9964755/e1c52bc8278f/ijms-24-04120-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0747/9964755/8041b46bb7e8/ijms-24-04120-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0747/9964755/8d79a5a6ed24/ijms-24-04120-g003.jpg

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