Osteoclasts may play key roles in initiating vascular calcification during atherosclerosis

IF 1 4区 医学 Q3 MEDICINE, RESEARCH & EXPERIMENTAL
Medical hypotheses Pub Date : 2026-04-01 Epub Date: 2026-02-24 DOI:10.1016/j.mehy.2026.111928
Yuxiao Liu , Jingqi Wu , Jingrong Chen , Hongmei Zhang , Mingzheng Li
{"title":"Osteoclasts may play key roles in initiating vascular calcification during atherosclerosis","authors":"Yuxiao Liu ,&nbsp;Jingqi Wu ,&nbsp;Jingrong Chen ,&nbsp;Hongmei Zhang ,&nbsp;Mingzheng Li","doi":"10.1016/j.mehy.2026.111928","DOIUrl":null,"url":null,"abstract":"<div><div>Vascular calcification, characterized by the ectopic deposition of calcium and phosphate crystals or even bone-like tissue, is a major risk factor for cardiovascular diseases such as atherosclerosis. However, the explicit mechanism remains unsettled. Current research demonstrates that atherosclerotic vascular calcification is a form of extraskeletal ossification—an active, cell-mediated process that closely resembles bone from macroscopic features down to the nanoscale structure. The mechanism underlying atherosclerotic calcification may be remarkably similar to those regulating bone remodeling and biomaterials-induced heterotopic ossification. This similarity is notably evidenced by the presence of osteoclast-like cells within vascular plaques. Based on previous findings that osteoclasts play key roles in initiating biomaterial-induced heterotopic ossification, we hypothesize for the first time that osteoclasts formed within the vascular wall may act as an ‘initiating signal’ triggering the development of atherosclerotic vascular calcification. This perspective may open new avenues for research into atherosclerotic calcification and contribute to the future development of strategies for its prevention and treatment.</div></div>","PeriodicalId":18425,"journal":{"name":"Medical hypotheses","volume":"209 ","pages":"Article 111928"},"PeriodicalIF":1.0000,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Medical hypotheses","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0306987726000575","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2026/2/24 0:00:00","PubModel":"Epub","JCR":"Q3","JCRName":"MEDICINE, RESEARCH & EXPERIMENTAL","Score":null,"Total":0}
引用次数: 0

Abstract

Vascular calcification, characterized by the ectopic deposition of calcium and phosphate crystals or even bone-like tissue, is a major risk factor for cardiovascular diseases such as atherosclerosis. However, the explicit mechanism remains unsettled. Current research demonstrates that atherosclerotic vascular calcification is a form of extraskeletal ossification—an active, cell-mediated process that closely resembles bone from macroscopic features down to the nanoscale structure. The mechanism underlying atherosclerotic calcification may be remarkably similar to those regulating bone remodeling and biomaterials-induced heterotopic ossification. This similarity is notably evidenced by the presence of osteoclast-like cells within vascular plaques. Based on previous findings that osteoclasts play key roles in initiating biomaterial-induced heterotopic ossification, we hypothesize for the first time that osteoclasts formed within the vascular wall may act as an ‘initiating signal’ triggering the development of atherosclerotic vascular calcification. This perspective may open new avenues for research into atherosclerotic calcification and contribute to the future development of strategies for its prevention and treatment.
破骨细胞可能在动脉粥样硬化期间启动血管钙化中起关键作用
血管钙化以钙和磷酸盐晶体甚至骨样组织的异位沉积为特征,是动脉粥样硬化等心血管疾病的主要危险因素。然而,明确的机制仍未解决。目前的研究表明,动脉粥样硬化性血管钙化是骨骼外骨化的一种形式——一种活跃的、细胞介导的过程,从宏观特征到纳米级结构都与骨骼非常相似。动脉粥样硬化钙化的机制可能与调节骨重塑和生物材料诱导的异位骨化非常相似。血管斑块内存在的破骨细胞样细胞明显证明了这种相似性。基于先前的研究结果,破骨细胞在启动生物材料诱导的异位骨化中起关键作用,我们首次假设血管壁内形成的破骨细胞可能作为触发动脉粥样硬化性血管钙化发展的“启动信号”。这一观点可能为动脉粥样硬化性钙化的研究开辟新的途径,并有助于未来预防和治疗策略的发展。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
Medical hypotheses
Medical hypotheses 医学-医学:研究与实验
CiteScore
10.60
自引率
2.10%
发文量
167
审稿时长
60 days
期刊介绍: Medical Hypotheses is a forum for ideas in medicine and related biomedical sciences. It will publish interesting and important theoretical papers that foster the diversity and debate upon which the scientific process thrives. The Aims and Scope of Medical Hypotheses are no different now from what was proposed by the founder of the journal, the late Dr David Horrobin. In his introduction to the first issue of the Journal, he asks ''what sorts of papers will be published in Medical Hypotheses? and goes on to answer ''Medical Hypotheses will publish papers which describe theories, ideas which have a great deal of observational support and some hypotheses where experimental support is yet fragmentary''. (Horrobin DF, 1975 Ideas in Biomedical Science: Reasons for the foundation of Medical Hypotheses. Medical Hypotheses Volume 1, Issue 1, January-February 1975, Pages 1-2.). Medical Hypotheses was therefore launched, and still exists today, to give novel, radical new ideas and speculations in medicine open-minded consideration, opening the field to radical hypotheses which would be rejected by most conventional journals. Papers in Medical Hypotheses take a standard scientific form in terms of style, structure and referencing. The journal therefore constitutes a bridge between cutting-edge theory and the mainstream of medical and scientific communication, which ideas must eventually enter if they are to be critiqued and tested against observations.
×
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:604180095
Book学术官方微信
小红书