Exploration and breakthrough in the mode of intervertebral disc cell death may lead to significant advances in treatments for intervertebral disc degeneration.

IF 2.8 3区 医学 Q1 ORTHOPEDICS Journal of Orthopaedic Surgery and Research Pub Date : 2024-12-05 DOI:10.1186/s13018-024-05280-z
Heng Chen, Tian Tang, Congyang Xue, Xin Liu, Zhipeng Xi, Lin Xie, Ran Kang
{"title":"Exploration and breakthrough in the mode of intervertebral disc cell death may lead to significant advances in treatments for intervertebral disc degeneration.","authors":"Heng Chen, Tian Tang, Congyang Xue, Xin Liu, Zhipeng Xi, Lin Xie, Ran Kang","doi":"10.1186/s13018-024-05280-z","DOIUrl":null,"url":null,"abstract":"<p><p>Low back pain caused by intervertebral disc degeneration (IDD) has emerged as a significant global public health concern, with far-reaching consequences for patients' quality of life and healthcare systems. Although previous research have revealed that the mechanisms of intervertebral disc cell apoptosis, pyroptosis and necroptosis can aggravate IDD damage by mediating inflammation and promoting extracellular matrix degradation, but they cannot explain the connection between different cell death mechanisms and ion metabolism disorders. The latest study shows that cell death mechanisms such as cellular senescence, ferroptosis, and cuproptosis, and PANopotosis have similar roles in the progression of intervertebral disc degeneration, but not exactly the same damage mechanism. This paper summarizes the effects of various cell death patterns on the disease progression of IDD, related molecular mechanisms and signaling pathways, providing new perspectives and potential clinical intervention strategies for the prevention and treatment of IDD.</p>","PeriodicalId":16629,"journal":{"name":"Journal of Orthopaedic Surgery and Research","volume":"19 1","pages":"825"},"PeriodicalIF":2.8000,"publicationDate":"2024-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11619685/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Orthopaedic Surgery and Research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1186/s13018-024-05280-z","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"ORTHOPEDICS","Score":null,"Total":0}
引用次数: 0

Abstract

Low back pain caused by intervertebral disc degeneration (IDD) has emerged as a significant global public health concern, with far-reaching consequences for patients' quality of life and healthcare systems. Although previous research have revealed that the mechanisms of intervertebral disc cell apoptosis, pyroptosis and necroptosis can aggravate IDD damage by mediating inflammation and promoting extracellular matrix degradation, but they cannot explain the connection between different cell death mechanisms and ion metabolism disorders. The latest study shows that cell death mechanisms such as cellular senescence, ferroptosis, and cuproptosis, and PANopotosis have similar roles in the progression of intervertebral disc degeneration, but not exactly the same damage mechanism. This paper summarizes the effects of various cell death patterns on the disease progression of IDD, related molecular mechanisms and signaling pathways, providing new perspectives and potential clinical intervention strategies for the prevention and treatment of IDD.

Abstract Image

Abstract Image

Abstract Image

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
对椎间盘细胞死亡模式的探索和突破可能会导致椎间盘退变的治疗取得重大进展。
椎间盘退变(IDD)引起的腰痛已成为一个重大的全球公共卫生问题,对患者的生活质量和医疗保健系统产生深远的影响。虽然已有研究揭示了椎间盘细胞凋亡、焦亡和坏死的机制可通过介导炎症和促进细胞外基质降解等方式加重IDD损伤,但不能解释不同细胞死亡机制与离子代谢紊乱之间的联系。最新研究表明,细胞衰老、铁下垂、铜下垂和PANopotosis等细胞死亡机制在椎间盘退变的进展中具有相似的作用,但其损伤机制并不完全相同。本文综述了各种细胞死亡模式对IDD疾病进展的影响、相关分子机制和信号通路,为IDD的防治提供了新的视角和潜在的临床干预策略。
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 去求助
来源期刊
CiteScore
4.10
自引率
7.70%
发文量
494
审稿时长
>12 weeks
期刊介绍: Journal of Orthopaedic Surgery and Research is an open access journal that encompasses all aspects of clinical and basic research studies related to musculoskeletal issues. Orthopaedic research is conducted at clinical and basic science levels. With the advancement of new technologies and the increasing expectation and demand from doctors and patients, we are witnessing an enormous growth in clinical orthopaedic research, particularly in the fields of traumatology, spinal surgery, joint replacement, sports medicine, musculoskeletal tumour management, hand microsurgery, foot and ankle surgery, paediatric orthopaedic, and orthopaedic rehabilitation. The involvement of basic science ranges from molecular, cellular, structural and functional perspectives to tissue engineering, gait analysis, automation and robotic surgery. Implant and biomaterial designs are new disciplines that complement clinical applications. JOSR encourages the publication of multidisciplinary research with collaboration amongst clinicians and scientists from different disciplines, which will be the trend in the coming decades.
期刊最新文献
Association between baseline lipid levels and re-fracture after percutaneous vertebroplasty for osteoporotic vertebral compression fractures: a retrospective cohort study. Efficacy and safety of combined supra-inguinal fascia iliaca compartment block and sacral plexus block versus spinal anesthesia in elderly patients undergoing hip fracture surgery: a prospective randomized controlled trial. Impact of flexion contracture severity on early outcomes of computer-navigated total knee arthroplasty: a retrospective cohort study. A comparative study of the clinical value of PRP and microfracture techniques in the repair of rotator cuff injuries. Clinical study on the reduction of perioperative blood loss in primary total hip arthroplasty by local application of hemocoagulase bothrops atrox for injection: a randomized controlled trial.
×
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学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:604180095
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