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骨硬化蛋白3A与骨质疏松症:文献综述

Semaphorin 3A on Osteoporosis: An Overreview of the Literature.

作者信息

Zhang Yueyi, Shi Hanfen, Dai Xuan, Shen Jin, Yin Jiyuan, Xu Tianshu, Yue Gaiyue, Guo Haochen, Liang Ruiqiong, Chen Qishuang, Gao Sihua, Wang Lili, Zhang Dongwei

机构信息

Traditional Chinese Medicine School, Diabetes Research Center, Beijing University of Chinese Medicine, Beijing, 100029, China.

Department of TCM Pharmacology, Chinese Material Medica School, Beijing University of Chinese Medicine, Beijing, 102488, China.

出版信息

Calcif Tissue Int. 2025 Feb 22;116(1):43. doi: 10.1007/s00223-025-01350-4.

DOI:10.1007/s00223-025-01350-4
PMID:39985619
Abstract

Semaphorin 3A (Sema3A) is a signaling protein that has attracted increasing attention in recent years for its important role in regulating bone metabolism. In this review, we searched different databases with various combinations of keywords to analyze the effects of Sema3A on osteoporosis. Sema3A promotes bone formation and inhibits bone resorption by directly affecting the osteoblast and osteoclast or indirectly targeting the nervous system. The sympathetic nervous system may be the main link between the central nervous system and bone metabolism for Sema3A. In the peripheral nervous system, Sema3A may improve bone quality via sensory nervous innervation. In addition, estrogen is found to regulate Sema3A levels to improve bone homeostasis. Lots of Sema3A agonists have been documented to exhibit anti-osteoporotic potential in preclinical investigations. Therefore, Sema3A can be considered a novel therapeutic target for preserving bone mass, highlighting an alternative strategy for the development of anti-osteoporosis drugs.

摘要

信号素3A(Sema3A)是一种信号蛋白,近年来因其在调节骨代谢中的重要作用而受到越来越多的关注。在本综述中,我们用各种关键词组合搜索了不同的数据库,以分析Sema3A对骨质疏松症的影响。Sema3A通过直接影响成骨细胞和破骨细胞或间接作用于神经系统来促进骨形成并抑制骨吸收。交感神经系统可能是Sema3A在中枢神经系统和骨代谢之间的主要联系环节。在周围神经系统中,Sema3A可能通过感觉神经支配来改善骨质量。此外,发现雌激素可调节Sema3A水平以改善骨稳态。许多Sema3A激动剂在临床前研究中已被证明具有抗骨质疏松的潜力。因此,Sema3A可被视为一种用于维持骨量的新型治疗靶点,为抗骨质疏松药物的开发突出了一种替代策略。

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本文引用的文献

1
Sema3A secreted by sensory nerve induces bone formation under mechanical loads.感觉神经分泌的 Sema3A 在机械负荷下诱导骨形成。
Int J Oral Sci. 2024 Jan 19;16(1):5. doi: 10.1038/s41368-023-00269-6.
2
The effects of semaphorin 3A in bone and cartilage metabolism: fundamental mechanism and clinical potential.信号素3A在骨与软骨代谢中的作用:基本机制及临床潜力
Front Cell Dev Biol. 2023 Nov 23;11:1321151. doi: 10.3389/fcell.2023.1321151. eCollection 2023.
3
SiJunZi decoction ameliorates bone quality and redox homeostasis and regulates advanced glycation end products/receptor for advanced glycation end products and WNT/β-catenin signaling pathways in diabetic mice.
四君子汤改善糖尿病小鼠的骨质量和氧化还原稳态,并调节晚期糖基化终产物/晚期糖基化终产物受体和 WNT/β-连环蛋白信号通路。
J Ethnopharmacol. 2024 Jan 30;319(Pt 2):117167. doi: 10.1016/j.jep.2023.117167. Epub 2023 Sep 14.
4
Postmenopausal osteoporosis coexisting with sarcopenia: the role and mechanisms of estrogen.绝经后骨质疏松症与肌肉减少症共存:雌激素的作用及机制
J Endocrinol. 2023 Sep 11;259(1). doi: 10.1530/JOE-23-0116. Print 2023 Sep 1.
5
miR-196b-5p Regulates Osteoblast and Osteoclast Differentiation and Bone Homeostasis by Targeting SEMA3A.miR-196b-5p 通过靶向 SEMA3A 调节成骨细胞和破骨细胞分化及骨稳态。
J Bone Miner Res. 2023 Aug;38(8):1175-1191. doi: 10.1002/jbmr.4834. Epub 2023 Jun 8.
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Progress of Wnt Signaling Pathway in Osteoporosis.Wnt 信号通路在骨质疏松症中的研究进展。
Biomolecules. 2023 Mar 6;13(3):483. doi: 10.3390/biom13030483.
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l-Type amino acid transporter 1 in hypothalamic neurons in mice maintains energy and bone homeostasis.l 型氨基酸转运蛋白 1 在小鼠下丘脑神经元中维持能量和骨骼内稳态。
JCI Insight. 2023 Apr 10;8(7):e154925. doi: 10.1172/jci.insight.154925.
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The role of sensory and sympathetic nerves in craniofacial bone regeneration.感觉神经和交感神经在颅面骨再生中的作用。
Neuropeptides. 2023 Jun;99:102328. doi: 10.1016/j.npep.2023.102328. Epub 2023 Feb 18.
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Inhibits Alveolar Bone Destruction in a Rat Model with Lipopolysaccharide (LPS)-Induced Periodontitis.在脂多糖(LPS)诱导的大鼠牙周炎模型中抑制牙槽骨破坏。
Int J Dent. 2022 Dec 30;2022:7398924. doi: 10.1155/2022/7398924. eCollection 2022.
10
RANKL-responsive epigenetic mechanism reprograms macrophages into bone-resorbing osteoclasts.RANKL 反应性表观遗传机制将巨噬细胞重编程为骨吸收破骨细胞。
Cell Mol Immunol. 2023 Jan;20(1):94-109. doi: 10.1038/s41423-022-00959-x. Epub 2022 Dec 14.