文献检索文档翻译深度研究
Suppr Zotero 插件Zotero 插件
邀请有礼套餐&价格历史记录

新学期，新优惠

限时优惠:9月1日-9月22日

30天高级会员仅需29元

1天体验卡首发特惠仅需5.99元

了解详情
不再提醒
插件&应用
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
高级版
套餐订阅购买积分包
AI 工具
文献检索文档翻译深度研究
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利：CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2025

中和过量的活性转化生长因子-β1可减少间充质干细胞的募集和分化，以减轻腱周粘连。

Neutralization of excessive levels of active TGF-β1 reduces MSC recruitment and differentiation to mitigate peritendinous adhesion.

作者信息

Li YuSheng, Wang Xiao, Hu Bo, Sun Qi, Wan Mei, Carr Andrew, Liu Shen, Cao Xu

机构信息

Department of Orthopedic Surgery, The Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA.

Nuffield Department of Orthopedics, Rheumatology and Musculoskeletal Sciences, Botnar Research Centre, University of Oxford, Windmill Road, Oxford, OX3 7LD, UK.

出版信息

Bone Res. 2023 May 8;11(1):24. doi: 10.1038/s41413-023-00252-1.

DOI:10.1038/s41413-023-00252-1
PMID:37156778
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10167238/
Abstract

Peritendinous adhesion formation (PAF) can substantially limit the range of motion of digits. However, the origin of myofibroblasts in PAF tissues is still unclear. In this study, we found that the concentration of active TGF-β1 and the numbers of macrophages, mesenchymal stromal cells (MSCs), and myofibroblasts in human and mouse adhesion tissues were increased. Furthermore, knockout of TGF-β1 in macrophages or TGF-β1R2 in MSCs inhibited PAF by reducing MSC and myofibroblast infiltration and collagen I and III deposition, respectively. Moreover, we found that MSCs differentiated into myofibroblasts to form adhesion tissues. Systemic injection of the TGF-β-neutralizing antibody 1D11 during the granulation formation stage of PAF significantly reduced the infiltration of MSCs and myofibroblasts and, subsequently, PAF. These results suggest that macrophage-derived TGF-β1 recruits MSCs to form myofibroblasts in peritendinous adhesions. An improved understanding of PAF mechanisms could help identify a potential therapeutic strategy.

摘要

腱周粘连形成（PAF）可显著限制手指的活动范围。然而，PAF组织中肌成纤维细胞的来源仍不清楚。在本研究中，我们发现人和小鼠粘连组织中活性转化生长因子-β1（TGF-β1）的浓度以及巨噬细胞、间充质基质细胞（MSC）和肌成纤维细胞的数量均增加。此外，巨噬细胞中TGF-β1基因敲除或MSC中TGF-β1R2基因敲除分别通过减少MSC和肌成纤维细胞浸润以及I型和III型胶原沉积来抑制PAF。此外，我们发现MSC分化为肌成纤维细胞以形成粘连组织。在PAF肉芽形成阶段全身注射TGF-β中和抗体1D11可显著减少MSC和肌成纤维细胞的浸润，进而减少PAF。这些结果表明，巨噬细胞来源的TGF-β1募集MSC以在腱周粘连中形成肌成纤维细胞。对PAF机制的深入了解有助于确定潜在的治疗策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5dd7/10167238/e574fcbe9cf7/41413_2023_252_Fig11_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5dd7/10167238/33b806ac7baf/41413_2023_252_Sch1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5dd7/10167238/3befd81aac08/41413_2023_252_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5dd7/10167238/7889ee5cc9f3/41413_2023_252_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5dd7/10167238/73f99498f738/41413_2023_252_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5dd7/10167238/5cfb140d8008/41413_2023_252_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5dd7/10167238/9ac3bd850f10/41413_2023_252_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5dd7/10167238/8e6c17a10979/41413_2023_252_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5dd7/10167238/194e0e3ee2ee/41413_2023_252_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5dd7/10167238/486d8f34a890/41413_2023_252_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5dd7/10167238/d8d76dc1efb8/41413_2023_252_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5dd7/10167238/0cc64eeda19f/41413_2023_252_Fig10_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5dd7/10167238/e574fcbe9cf7/41413_2023_252_Fig11_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5dd7/10167238/33b806ac7baf/41413_2023_252_Sch1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5dd7/10167238/3befd81aac08/41413_2023_252_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5dd7/10167238/7889ee5cc9f3/41413_2023_252_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5dd7/10167238/73f99498f738/41413_2023_252_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5dd7/10167238/5cfb140d8008/41413_2023_252_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5dd7/10167238/9ac3bd850f10/41413_2023_252_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5dd7/10167238/8e6c17a10979/41413_2023_252_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5dd7/10167238/194e0e3ee2ee/41413_2023_252_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5dd7/10167238/486d8f34a890/41413_2023_252_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5dd7/10167238/d8d76dc1efb8/41413_2023_252_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5dd7/10167238/0cc64eeda19f/41413_2023_252_Fig10_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5dd7/10167238/e574fcbe9cf7/41413_2023_252_Fig11_HTML.jpg

相似文献

[1]
Neutralization of excessive levels of active TGF-β1 reduces MSC recruitment and differentiation to mitigate peritendinous adhesion.

Bone Res. 2023-5-8

[2]
Intrinsic Deregulation of Vascular Smooth Muscle and Myofibroblast Differentiation in Mesenchymal Stromal Cells from Patients with Systemic Sclerosis.

PLoS One. 2016-4-7

[3]
Hyaluronan Controls the Deposition of Fibronectin and Collagen and Modulates TGF-β1 Induction of Lung Myofibroblasts.

Matrix Biol. 2015-3

[4]
RUNX1 is essential for mesenchymal stem cell proliferation and myofibroblast differentiation.

Proc Natl Acad Sci U S A. 2014-11-18

[5]
Human umbilical cord mesenchymal stem cell-derived exosomes suppress dermal fibroblasts-myofibroblats transition via inhibiting the TGF-β1/Smad 2/3 signaling pathway.

Exp Mol Pathol. 2020-5-21

[6]
Overexpressing TGF-β1 in mesenchymal stem cells attenuates organ dysfunction during CLP-induced septic mice by reducing macrophage-driven inflammation.

Stem Cell Res Ther. 2020-9-3

[7]
Endometriotic mesenchymal stem cells significantly promote fibrogenesis in ovarian endometrioma through the Wnt/β-catenin pathway by paracrine production of TGF-β1 and Wnt1.

Hum Reprod. 2016-6

[8]
Mesenchymal stem cells reversibly de-differentiate myofibroblasts to fibroblast-like cells by inhibiting the TGF-β-SMAD2/3 pathway.

Mol Med. 2023-4-25

[9]
Functional effects of TGF-β1 on mesenchymal stem cell mobilization in cockroach allergen-induced asthma.

J Immunol. 2014-4-7

[10]
Platelet-Rich Plasma and Bone Marrow-Derived Mesenchymal Stromal Cells Prevent TGF-β1-Induced Myofibroblast Generation but Are Not Synergistic when Combined: Morphological in vitro Analysis.

Cells Tissues Organs. 2018

引用本文的文献

[1]
Screening of hub genes and immunocytes related to tendon injury based on bioinformatics and machine learning models.

Sci Rep. 2025-8-26

[2]
Healing of tendon-related diseases: insights from macrophage regulation.

Mil Med Res. 2025-8-4

[3]
The role of MicroRNAs in mesenchymal stem cell differentiation into vascular smooth muscle cells.

Cell Div. 2025-3-7

[4]
Digging into the Cause of Abnormal Patellar Kinematics After Open-Wedge High Tibial Osteotomy via a Quantitative Study on In Vivo Soft Tissue Functional Changes.

Bioengineering (Basel). 2025-1-28

[5]
Challenges in tendon-bone healing: emphasizing inflammatory modulation mechanisms and treatment.

Front Endocrinol (Lausanne). 2024

[6]
Human Tendon-on-a-Chip for Modeling the Myofibroblast Microenvironment in Peritendinous Fibrosis.

Adv Healthc Mater. 2025-2

[7]
Myeloid Cells and Sensory Nerves Mediate Peritendinous Adhesion Formation via Prostaglandin E2.

Adv Sci (Weinh). 2024-10

[8]
Multi-omics analysis of human tendon adhesion reveals that ACKR1-regulated macrophage migration is involved in regeneration.

Bone Res. 2024-5-7

[9]
Diamond-Like Carbon Depositing on the Surface of Polylactide Membrane for Prevention of Adhesion Formation During Tendon Repair.

Nanomicro Lett. 2024-4-30

[10]
TGF-β signaling in health, disease, and therapeutics.

Signal Transduct Target Ther. 2024-3-22

本文引用的文献

[1]
Sialylation of TLR2 initiates osteoclast fusion.

Bone Res. 2022-3-2

[2]
Tenolysis rate after zone 2 flexor tendon repairs.

Jt Dis Relat Surg. 2020

[3]
The use of 5-fluorouracil in the prevention of tendon adhesions: A systematic review.

Animal Model Exp Med. 2020-4-3

[4]
Follistatin Mitigates Myofibroblast Differentiation and Collagen Synthesis of Fibroblasts from Scar Tissue around Injured Flexor Tendons.

Yonsei Med J. 2020-1

[5]
Flexor Tendon: Development, Healing, Adhesion Formation, and Contributing Growth Factors.

Plast Reconstr Surg. 2019-10

[6]
Use of a supramolecular polymeric hydrogel as an effective post-operative pericardial adhesion barrier.

Nat Biomed Eng. 2019-8-7

[7]
Deletion of NFKB1 enhances canonical NF-κB signaling and increases macrophage and myofibroblast content during tendon healing.

Sci Rep. 2019-7-29

[8]
Prevention of postoperative adhesion reformation by intermittent intrauterine balloon therapy: a randomised controlled trial.

BJOG. 2019-7-18

[9]
Biological Amnion Prevents Flexor Tendon Adhesion in Zone II: A Controlled, Multicentre Clinical Trial.

Biomed Res Int. 2019-4-3

[10]
The cellular basis of fibrotic tendon healing: challenges and opportunities.

Transl Res. 2019-2-8

文献AI研究员

20分钟写一篇综述，助力文献阅读效率提升50倍

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

推荐工具

医学文档翻译智能文献检索