生物钟基因Bmal1调控骨和软骨代谢的信号通路机制综述

IF 14.3 1区 医学 Q1 CELL & TISSUE ENGINEERING
Yiting Ze, Yongyao Wu, Zhen Tan, Rui Li, Rong Li, Wenzhen Gao, Qing Zhao
{"title":"生物钟基因Bmal1调控骨和软骨代谢的信号通路机制综述","authors":"Yiting Ze, Yongyao Wu, Zhen Tan, Rui Li, Rong Li, Wenzhen Gao, Qing Zhao","doi":"10.1038/s41413-025-00403-6","DOIUrl":null,"url":null,"abstract":"<p>Circadian rhythm is ubiquitous in nature. Circadian clock genes such as <i>Bmal1</i> and <i>Clock</i> form a multi-level transcription-translation feedback network, and regulate a variety of physiological and pathological processes, including bone and cartilage metabolism. Deletion of the core clock gene <i>Bmal1</i> leads to pathological bone alterations, while the phenotypes are not consistent. Studies have shown that multiple signaling pathways are involved in the process of <i>Bmal1</i> regulating bone and cartilage metabolism, but the exact regulatory mechanisms remain unclear. This paper reviews the signaling pathways by which <i>Bmal1</i> regulates bone/cartilage metabolism, the upstream regulatory factors that control <i>Bmal1</i>, and the current <i>Bmal1</i> knockout mouse models for research. We hope to provide new insights for the prevention and treatment of bone/cartilage diseases related to circadian rhythms.</p>","PeriodicalId":9134,"journal":{"name":"Bone Research","volume":"7 1","pages":""},"PeriodicalIF":14.3000,"publicationDate":"2025-01-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Signaling pathway mechanisms of circadian clock gene Bmal1 regulating bone and cartilage metabolism: a review\",\"authors\":\"Yiting Ze, Yongyao Wu, Zhen Tan, Rui Li, Rong Li, Wenzhen Gao, Qing Zhao\",\"doi\":\"10.1038/s41413-025-00403-6\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p>Circadian rhythm is ubiquitous in nature. Circadian clock genes such as <i>Bmal1</i> and <i>Clock</i> form a multi-level transcription-translation feedback network, and regulate a variety of physiological and pathological processes, including bone and cartilage metabolism. Deletion of the core clock gene <i>Bmal1</i> leads to pathological bone alterations, while the phenotypes are not consistent. Studies have shown that multiple signaling pathways are involved in the process of <i>Bmal1</i> regulating bone and cartilage metabolism, but the exact regulatory mechanisms remain unclear. This paper reviews the signaling pathways by which <i>Bmal1</i> regulates bone/cartilage metabolism, the upstream regulatory factors that control <i>Bmal1</i>, and the current <i>Bmal1</i> knockout mouse models for research. We hope to provide new insights for the prevention and treatment of bone/cartilage diseases related to circadian rhythms.</p>\",\"PeriodicalId\":9134,\"journal\":{\"name\":\"Bone Research\",\"volume\":\"7 1\",\"pages\":\"\"},\"PeriodicalIF\":14.3000,\"publicationDate\":\"2025-01-27\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Bone Research\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1038/s41413-025-00403-6\",\"RegionNum\":1,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"CELL & TISSUE ENGINEERING\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Bone Research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1038/s41413-025-00403-6","RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"CELL & TISSUE ENGINEERING","Score":null,"Total":0}
引用次数: 0

摘要

昼夜节律在自然界中无处不在。Bmal1和clock等生物钟基因形成了一个多层次的转录-翻译反馈网络,并调节多种生理和病理过程,包括骨和软骨代谢。核心时钟基因Bmal1的缺失导致病理性骨改变,而表型不一致。研究表明,Bmal1调节骨和软骨代谢的过程涉及多种信号通路,但确切的调节机制尚不清楚。本文综述了Bmal1调节骨/软骨代谢的信号通路、控制Bmal1的上游调控因子以及目前研究的Bmal1敲除小鼠模型。我们希望为预防和治疗与昼夜节律相关的骨/软骨疾病提供新的见解。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Signaling pathway mechanisms of circadian clock gene Bmal1 regulating bone and cartilage metabolism: a review

Signaling pathway mechanisms of circadian clock gene Bmal1 regulating bone and cartilage metabolism: a review

Circadian rhythm is ubiquitous in nature. Circadian clock genes such as Bmal1 and Clock form a multi-level transcription-translation feedback network, and regulate a variety of physiological and pathological processes, including bone and cartilage metabolism. Deletion of the core clock gene Bmal1 leads to pathological bone alterations, while the phenotypes are not consistent. Studies have shown that multiple signaling pathways are involved in the process of Bmal1 regulating bone and cartilage metabolism, but the exact regulatory mechanisms remain unclear. This paper reviews the signaling pathways by which Bmal1 regulates bone/cartilage metabolism, the upstream regulatory factors that control Bmal1, and the current Bmal1 knockout mouse models for research. We hope to provide new insights for the prevention and treatment of bone/cartilage diseases related to circadian rhythms.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
Bone Research
Bone Research CELL & TISSUE ENGINEERING-
CiteScore
20.00
自引率
4.70%
发文量
289
审稿时长
20 weeks
期刊介绍: Established in 2013, Bone Research is a newly-founded English-language periodical that centers on the basic and clinical facets of bone biology, pathophysiology, and regeneration. It is dedicated to championing key findings emerging from both basic investigations and clinical research concerning bone-related topics. The journal's objective is to globally disseminate research in bone-related physiology, pathology, diseases, and treatment, contributing to the advancement of knowledge in this field.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信