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本文引用的文献

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Excessive mechanical loading promotes osteoarthritis through the gremlin-1-NF-κB pathway.过度的机械负荷通过 Gremlin-1-NF-κB 通路促进骨关节炎。
Nat Commun. 2019 Mar 29;10(1):1442. doi: 10.1038/s41467-019-09491-5.
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Morphogenetic mechanism of the acquisition of the dinosaur-type acetabulum.恐龙型髋臼形成的形态发生机制。
R Soc Open Sci. 2018 Oct 17;5(10):180604. doi: 10.1098/rsos.180604. eCollection 2018 Oct.
3
Disease-modifying drugs in osteoarthritis: current understanding and future therapeutics.骨关节炎的疾病修饰药物:现有认识与未来治疗策略。
Expert Opin Emerg Drugs. 2018 Dec;23(4):331-347. doi: 10.1080/14728214.2018.1547706. Epub 2018 Dec 3.
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miR-324-5p is up regulated in end-stage osteoarthritis and regulates Indian Hedgehog signalling by differing mechanisms in human and mouse.miR-324-5p 在终末期骨关节炎中上调,并通过不同的机制在人和小鼠中调节 Indian Hedgehog 信号通路。
Matrix Biol. 2019 Apr;77:87-100. doi: 10.1016/j.matbio.2018.08.009. Epub 2018 Sep 5.
5
Regulation of lubricin for functional cartilage tissue regeneration: a review.润滑素对功能性软骨组织再生的调节作用:综述
Biomater Res. 2018 Mar 16;22:9. doi: 10.1186/s40824-018-0118-x. eCollection 2018.
6
Precise spatial restriction of BMP signaling in developing joints is perturbed upon loss of embryo movement.胚胎运动缺失时,发育关节中骨形态发生蛋白信号的精确空间限制会受到干扰。
Development. 2018 Mar 12;145(5):dev153460. doi: 10.1242/dev.153460.
7
FoxO transcription factors modulate autophagy and proteoglycan 4 in cartilage homeostasis and osteoarthritis.FoxO 转录因子调节软骨稳态和骨关节炎中的自噬和蛋白聚糖 4。
Sci Transl Med. 2018 Feb 14;10(428). doi: 10.1126/scitranslmed.aan0746.
8
NFIA and GATA3 are crucial regulators of embryonic articular cartilage differentiation.NFIA和GATA3是胚胎关节软骨分化的关键调节因子。
Development. 2018 Jan 17;145(2):dev156554. doi: 10.1242/dev.156554.
9
Characterization of Mesenchymal Stem Cell-Like Cells Derived From Human iPSCs via Neural Crest Development and Their Application for Osteochondral Repair.通过神经嵴发育从人诱导多能干细胞衍生的间充质干细胞样细胞的表征及其在骨软骨修复中的应用
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10
Basic Science of Articular Cartilage.关节软骨的基础科学
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滑膜关节和关节软骨发育的机制。

Mechanisms of synovial joint and articular cartilage development.

机构信息

Bone and Cartilage Regenerative Medicine, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-8655, Japan.

Sensory and Motor System Medicine, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-8655, Japan.

出版信息

Cell Mol Life Sci. 2019 Oct;76(20):3939-3952. doi: 10.1007/s00018-019-03191-5. Epub 2019 Jun 14.

DOI:10.1007/s00018-019-03191-5
PMID:31201464
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11105481/
Abstract

Articular cartilage is formed at the end of epiphyses in the synovial joint cavity and permanently contributes to the smooth movement of synovial joints. Most skeletal elements develop from transient cartilage by a biological process known as endochondral ossification. Accumulating evidence indicates that articular and growth plate cartilage are derived from different cell sources and that different molecules and signaling pathways regulate these two kinds of cartilage. As the first sign of joint development, the interzone emerges at the presumptive joint site within a pre-cartilage tissue. After that, joint cavitation occurs in the center of the interzone, and the cells in the interzone and its surroundings gradually form articular cartilage and the synovial joint. During joint development, the interzone cells continuously migrate out to the epiphyseal cartilage and the surrounding cells influx into the joint region. These complicated phenomena are regulated by various molecules and signaling pathways, including GDF5, Wnt, IHH, PTHrP, BMP, TGF-β, and FGF. Here, we summarize current literature and discuss the molecular mechanisms underlying joint formation and articular development.

摘要

关节软骨形成于滑膜关节腔的骨骺末端,为滑膜关节的平滑运动提供永久性贡献。大多数骨骼元素通过一种称为软骨内骨化的生物学过程从短暂的软骨发育而来。越来越多的证据表明,关节软骨和生长板软骨来自不同的细胞来源,不同的分子和信号通路调节这两种软骨。作为关节发育的第一个标志,在软骨前组织内的假定关节部位出现过渡区。之后,关节在过渡区的中心发生空化,过渡区及其周围的细胞逐渐形成关节软骨和滑膜关节。在关节发育过程中,过渡区细胞不断向外迁移到骺软骨,周围的细胞向内流入关节区域。这些复杂的现象受到各种分子和信号通路的调节,包括 GDF5、Wnt、IHH、PTHrP、BMP、TGF-β 和 FGF。在这里,我们总结了目前的文献,并讨论了关节形成和关节发育的分子机制。