生长板闭合和治疗干预。

IF 3.2 Q1 PEDIATRICS Clinical and Experimental Pediatrics Pub Date : 2024-11-01 Epub Date: 2024-10-28 DOI:10.3345/cep.2023.00346
Ja Hyang Cho, Hae Woon Jung, Kye Shik Shim
{"title":"生长板闭合和治疗干预。","authors":"Ja Hyang Cho, Hae Woon Jung, Kye Shik Shim","doi":"10.3345/cep.2023.00346","DOIUrl":null,"url":null,"abstract":"<p><p>Height gains result from longitudinal bone growth, which is largely dependent on chondrocyte differentiation and proliferation within the growth plates of long bones. The growth plate, that is, the epiphyseal plate, is divided into resting, proliferative, and hypertrophic zones according to chondrocyte characteristics. The differentiation potential of progenitor cells in the resting zone, continuous capacity for chondrocyte differentiation and proliferation within the proliferative zone, timely replacement by osteocytes, and calcification in the hypertrophic zone are the 3 main factors controlling longitudinal bone growth. Upon adequate longitudinal bone growth, growth plate senescence limits human body height. During growth plate senescence, progenitor cells within the resting zone are depleted, proliferative chondrocyte numbers decrease, and hypertrophic chondrocyte number and size decrease. After senescence, hypertrophic chondrocytes are replaced by osteocytes, the extracellular matrix is calcified and vascularized, the growth plate is closed, and longitudinal bone growth is complete. To date, gonadotropin-releasing hormone analogs, aromatase inhibitors, C-type natriuretic peptide analogs, and fibroblast growth factor receptor 3 inhibitors have been studied or used as therapeutic interventions to delay growth plate closure. Complex networks of cellular, genetic, paracrine, and endocrine signals are involved in growth plate closure. However, the detailed mechanisms of this process remain unclear. Further elucidation of these mechanisms will enable the development of new therapeutic modalities for the treatment of short stature, precocious puberty, and skeletal dysplasia.</p>","PeriodicalId":36018,"journal":{"name":"Clinical and Experimental Pediatrics","volume":" ","pages":"553-559"},"PeriodicalIF":3.2000,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11551597/pdf/","citationCount":"0","resultStr":"{\"title\":\"Growth plate closure and therapeutic interventions.\",\"authors\":\"Ja Hyang Cho, Hae Woon Jung, Kye Shik Shim\",\"doi\":\"10.3345/cep.2023.00346\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Height gains result from longitudinal bone growth, which is largely dependent on chondrocyte differentiation and proliferation within the growth plates of long bones. The growth plate, that is, the epiphyseal plate, is divided into resting, proliferative, and hypertrophic zones according to chondrocyte characteristics. The differentiation potential of progenitor cells in the resting zone, continuous capacity for chondrocyte differentiation and proliferation within the proliferative zone, timely replacement by osteocytes, and calcification in the hypertrophic zone are the 3 main factors controlling longitudinal bone growth. Upon adequate longitudinal bone growth, growth plate senescence limits human body height. During growth plate senescence, progenitor cells within the resting zone are depleted, proliferative chondrocyte numbers decrease, and hypertrophic chondrocyte number and size decrease. After senescence, hypertrophic chondrocytes are replaced by osteocytes, the extracellular matrix is calcified and vascularized, the growth plate is closed, and longitudinal bone growth is complete. To date, gonadotropin-releasing hormone analogs, aromatase inhibitors, C-type natriuretic peptide analogs, and fibroblast growth factor receptor 3 inhibitors have been studied or used as therapeutic interventions to delay growth plate closure. Complex networks of cellular, genetic, paracrine, and endocrine signals are involved in growth plate closure. However, the detailed mechanisms of this process remain unclear. Further elucidation of these mechanisms will enable the development of new therapeutic modalities for the treatment of short stature, precocious puberty, and skeletal dysplasia.</p>\",\"PeriodicalId\":36018,\"journal\":{\"name\":\"Clinical and Experimental Pediatrics\",\"volume\":\" \",\"pages\":\"553-559\"},\"PeriodicalIF\":3.2000,\"publicationDate\":\"2024-11-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11551597/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Clinical and Experimental Pediatrics\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.3345/cep.2023.00346\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2024/10/28 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q1\",\"JCRName\":\"PEDIATRICS\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Clinical and Experimental Pediatrics","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.3345/cep.2023.00346","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/10/28 0:00:00","PubModel":"Epub","JCR":"Q1","JCRName":"PEDIATRICS","Score":null,"Total":0}
引用次数: 0

摘要

身高的增长源于骨骼的纵向生长,而骨骼的纵向生长主要取决于长骨生长板内软骨细胞的分化和增殖。生长板(即骺板)根据软骨细胞的特征分为静止区、增殖区和肥厚区。静止区祖细胞的分化潜能、增殖区内软骨细胞的持续分化和增殖能力、骨细胞的及时替代以及肥厚区的钙化是控制骨骼纵向生长的三个主要因素。在骨骼纵向生长达到一定程度后,生长板的衰老会限制人的身高。在生长板衰老过程中,静止区内的祖细胞耗竭,增殖软骨细胞数量减少,肥大软骨细胞数量和体积缩小。衰老后,肥大软骨细胞被骨细胞取代,细胞外基质钙化和血管化,生长板闭合,纵向骨生长完成。迄今为止,已有促性腺激素释放激素类似物、芳香化酶抑制剂、C 型钠尿肽类似物和成纤维细胞生长因子受体 3 抑制剂被研究或用作延迟生长板闭合的治疗干预措施。生长板闭合涉及复杂的细胞、遗传、旁分泌和内分泌信号网络。然而,这一过程的详细机制仍不清楚。对这些机制的进一步研究将有助于开发治疗矮身材、性早熟和骨骼发育不良的新方法。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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
Growth plate closure and therapeutic interventions.

Height gains result from longitudinal bone growth, which is largely dependent on chondrocyte differentiation and proliferation within the growth plates of long bones. The growth plate, that is, the epiphyseal plate, is divided into resting, proliferative, and hypertrophic zones according to chondrocyte characteristics. The differentiation potential of progenitor cells in the resting zone, continuous capacity for chondrocyte differentiation and proliferation within the proliferative zone, timely replacement by osteocytes, and calcification in the hypertrophic zone are the 3 main factors controlling longitudinal bone growth. Upon adequate longitudinal bone growth, growth plate senescence limits human body height. During growth plate senescence, progenitor cells within the resting zone are depleted, proliferative chondrocyte numbers decrease, and hypertrophic chondrocyte number and size decrease. After senescence, hypertrophic chondrocytes are replaced by osteocytes, the extracellular matrix is calcified and vascularized, the growth plate is closed, and longitudinal bone growth is complete. To date, gonadotropin-releasing hormone analogs, aromatase inhibitors, C-type natriuretic peptide analogs, and fibroblast growth factor receptor 3 inhibitors have been studied or used as therapeutic interventions to delay growth plate closure. Complex networks of cellular, genetic, paracrine, and endocrine signals are involved in growth plate closure. However, the detailed mechanisms of this process remain unclear. Further elucidation of these mechanisms will enable the development of new therapeutic modalities for the treatment of short stature, precocious puberty, and skeletal dysplasia.

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
CiteScore
8.00
自引率
2.40%
发文量
88
审稿时长
60 weeks
期刊最新文献
Absolute versus functional iron deficiency. Characteristics of temper tantrums in 1-6-year-old children and impact on caregivers. Effect of high-frequency oscillatory ventilation with intermittent sigh breaths on carbon dioxide levels in neonates. Effect of metabolic syndrome on pulmonary dysfunction in children with asthma. Further research on impact of microplastics on children's health is essential to protecting future generations.
×
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