糖皮质激素诱发骨质疏松症的发病机制。

IF 9.3 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Cytokine & Growth Factor Reviews Pub Date : 2023-04-01 DOI:10.1016/j.cytogfr.2023.03.002
Meng Chen , Wenyu Fu , Huiyun Xu , Chuan-ju Liu
{"title":"糖皮质激素诱发骨质疏松症的发病机制。","authors":"Meng Chen ,&nbsp;Wenyu Fu ,&nbsp;Huiyun Xu ,&nbsp;Chuan-ju Liu","doi":"10.1016/j.cytogfr.2023.03.002","DOIUrl":null,"url":null,"abstract":"<div><p><span><span><span>Glucocorticoid<span><span> (GC) is one of the most prescribed medicines to treat various inflammatory and autoimmune diseases. However, high doses and long-term use of GCs lead to multiple adverse effects, particularly glucocorticoid-induced osteoporosis (GIO). Excessive GCs exert detrimental effects on bone cells, including </span>osteoblasts, </span></span>osteoclasts, and </span>osteocytes, leading to impaired bone formation and resorption. The actions of exogenous GCs are considered to be strongly cell-type and dose dependent. GC excess inhibits the proliferation and differentiation of osteoblasts and enhances the </span>apoptosis<span><span> of osteoblasts and osteocytes, eventually contributing to reduced bone formation. Effects of GC excess on osteoclasts mainly include enhanced osteoclastogenesis, increased lifespan and number of mature osteoclasts, and diminished osteoclast apoptosis, which result in increased </span>bone resorption. Furthermore, GCs have an impact on the secretion of bone cells, subsequently disturbing the process of osteoblastogenesis and osteoclastogenesis. This review provides timely update and summary of recent discoveries in the field of GIO, with a particular focus on the effects of exogenous GCs on bone cells and the crosstalk among them under GC excess.</span></p></div>","PeriodicalId":11132,"journal":{"name":"Cytokine & Growth Factor Reviews","volume":null,"pages":null},"PeriodicalIF":9.3000,"publicationDate":"2023-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10518688/pdf/","citationCount":"6","resultStr":"{\"title\":\"Pathogenic mechanisms of glucocorticoid-induced osteoporosis\",\"authors\":\"Meng Chen ,&nbsp;Wenyu Fu ,&nbsp;Huiyun Xu ,&nbsp;Chuan-ju Liu\",\"doi\":\"10.1016/j.cytogfr.2023.03.002\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><p><span><span><span>Glucocorticoid<span><span> (GC) is one of the most prescribed medicines to treat various inflammatory and autoimmune diseases. However, high doses and long-term use of GCs lead to multiple adverse effects, particularly glucocorticoid-induced osteoporosis (GIO). Excessive GCs exert detrimental effects on bone cells, including </span>osteoblasts, </span></span>osteoclasts, and </span>osteocytes, leading to impaired bone formation and resorption. The actions of exogenous GCs are considered to be strongly cell-type and dose dependent. GC excess inhibits the proliferation and differentiation of osteoblasts and enhances the </span>apoptosis<span><span> of osteoblasts and osteocytes, eventually contributing to reduced bone formation. Effects of GC excess on osteoclasts mainly include enhanced osteoclastogenesis, increased lifespan and number of mature osteoclasts, and diminished osteoclast apoptosis, which result in increased </span>bone resorption. Furthermore, GCs have an impact on the secretion of bone cells, subsequently disturbing the process of osteoblastogenesis and osteoclastogenesis. This review provides timely update and summary of recent discoveries in the field of GIO, with a particular focus on the effects of exogenous GCs on bone cells and the crosstalk among them under GC excess.</span></p></div>\",\"PeriodicalId\":11132,\"journal\":{\"name\":\"Cytokine & Growth Factor Reviews\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":9.3000,\"publicationDate\":\"2023-04-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10518688/pdf/\",\"citationCount\":\"6\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Cytokine & Growth Factor Reviews\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S1359610123000114\",\"RegionNum\":2,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"BIOCHEMISTRY & MOLECULAR BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cytokine & Growth Factor Reviews","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S1359610123000114","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
引用次数: 6

摘要

糖皮质激素(GC)是治疗各种炎症和自身免疫性疾病的最常用药物之一。然而,高剂量和长期使用GC会导致多种不良反应,特别是糖皮质激素诱导的骨质疏松症(GIO)。过量的GC对骨细胞(包括成骨细胞、破骨细胞和骨细胞)产生有害影响,导致骨形成和吸收受损。外源GC的作用被认为是强烈的细胞类型和剂量依赖性的。GC过量抑制成骨细胞的增殖和分化,增强成骨细胞和骨细胞的凋亡,最终导致骨形成减少。GC过量对破骨细胞的影响主要包括破骨细胞生成增强、成熟破骨细胞寿命和数量增加以及破骨细胞凋亡减少,从而导致骨吸收增加。此外,GC对骨细胞的分泌有影响,从而干扰成骨细胞和破骨细胞的生成过程。这篇综述及时更新和总结了GIO领域的最新发现,特别关注外源GC对骨细胞的影响以及在GC过量的情况下它们之间的串扰。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

摘要图片

查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
Pathogenic mechanisms of glucocorticoid-induced osteoporosis

Glucocorticoid (GC) is one of the most prescribed medicines to treat various inflammatory and autoimmune diseases. However, high doses and long-term use of GCs lead to multiple adverse effects, particularly glucocorticoid-induced osteoporosis (GIO). Excessive GCs exert detrimental effects on bone cells, including osteoblasts, osteoclasts, and osteocytes, leading to impaired bone formation and resorption. The actions of exogenous GCs are considered to be strongly cell-type and dose dependent. GC excess inhibits the proliferation and differentiation of osteoblasts and enhances the apoptosis of osteoblasts and osteocytes, eventually contributing to reduced bone formation. Effects of GC excess on osteoclasts mainly include enhanced osteoclastogenesis, increased lifespan and number of mature osteoclasts, and diminished osteoclast apoptosis, which result in increased bone resorption. Furthermore, GCs have an impact on the secretion of bone cells, subsequently disturbing the process of osteoblastogenesis and osteoclastogenesis. This review provides timely update and summary of recent discoveries in the field of GIO, with a particular focus on the effects of exogenous GCs on bone cells and the crosstalk among them under GC excess.

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
Cytokine & Growth Factor Reviews
Cytokine & Growth Factor Reviews 生物-生化与分子生物学
CiteScore
21.10
自引率
1.50%
发文量
61
审稿时长
22 days
期刊介绍: Cytokine & Growth Factor Reviews is a leading publication that focuses on the dynamic fields of growth factor and cytokine research. Our journal offers a platform for authors to disseminate thought-provoking articles such as critical reviews, state-of-the-art reviews, letters to the editor, and meeting reviews. We aim to cover important breakthroughs in these rapidly evolving areas, providing valuable insights into the multidisciplinary significance of cytokines and growth factors. Our journal spans various domains including signal transduction, cell growth and differentiation, embryonic development, immunology, tumorigenesis, and clinical medicine. By publishing cutting-edge research and analysis, we aim to influence the way researchers and experts perceive and understand growth factors and cytokines. We encourage novel expressions of ideas and innovative approaches to organizing content, fostering a stimulating environment for knowledge exchange and scientific advancement.
期刊最新文献
The role of transforming growth factor β in cervical carcinogenesis. Impact of chronic stress on intestinal mucosal immunity in colorectal cancer progression. Central role of Galectin-3 at the cross-roads of cardiac inflammation and fibrosis: Implications for heart failure and transplantation. Unraveling the intricacies of neutrophil extracellular traps in inflammatory bowel disease: Pathways, biomarkers, and promising therapies. Distinct roles of MIF in the pathogenesis of ischemic heart disease.
×
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
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 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 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1