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异位骨化中的成纤维细胞:机制与治疗靶点。

Fibroblasts in heterotopic ossification: mechanisms and therapeutic targets.

作者信息

Li Jia-Xin, Dang Yan-Miao, Liu Meng-Chao, Gao Lin-Qing, Lin Hui

机构信息

School of Basic Medical Sciences, Jiangxi Medical College, Nanchang University, Nanchang, 330006, China.

First Clinical School, Jiangxi Medical College, Nanchang University, Nanchang, 330006, China.

出版信息

Int J Biol Sci. 2025 Jan 1;21(2):544-564. doi: 10.7150/ijbs.102297. eCollection 2025.

DOI:10.7150/ijbs.102297
PMID:39781450
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11705629/
Abstract

Heterotopic ossification (HO) refers to the abnormal formation of bone in non-skeletal tissues. Fibroblasts have traditionally been viewed as stationary cells primarily responsible for producing extracellular matrix during tissue repair and fibrosis. However, recent discoveries regarding their plasticity-encompassing roles in inflammation, extracellular matrix remodeling, and osteogenesis-highlight their potential as key contributors to the development of HO. In this review, we systematically summarize the diverse phenotypic and functional plasticity of fibroblasts in HO. Furthermore, we evaluate the possible interaction between fibroblasts and macrophages in pathophysiological processes and signaling pathways. Finally, we highlight the potential strategies for preventing and treating HO by targeting fibroblast activities.

摘要

异位骨化(HO)是指在非骨骼组织中异常形成骨。传统上,成纤维细胞被视为静止细胞,主要负责在组织修复和纤维化过程中产生细胞外基质。然而,最近关于它们在炎症、细胞外基质重塑和成骨过程中具有可塑性的作用的发现,凸显了它们作为HO发展关键促成因素的潜力。在这篇综述中,我们系统地总结了HO中成纤维细胞多样的表型和功能可塑性。此外,我们评估了成纤维细胞与巨噬细胞在病理生理过程和信号通路中可能的相互作用。最后,我们强调了通过靶向成纤维细胞活性来预防和治疗HO的潜在策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b74/11705629/28783c15f811/ijbsv21p0544g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b74/11705629/5734af5d4626/ijbsv21p0544g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b74/11705629/281c10637737/ijbsv21p0544g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b74/11705629/a5a213879259/ijbsv21p0544g003.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b74/11705629/28783c15f811/ijbsv21p0544g005.jpg

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本文引用的文献

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Front Pharmacol. 2024 Jul 8;15:1434146. doi: 10.3389/fphar.2024.1434146. eCollection 2024.
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AMPK induces PIAS3 mediated SUMOylation of E3 ubiquitin ligase Smurf1 impairing osteogenic differentiation and traumatic heterotopic ossification.AMPK 诱导 PIAS3 介导的 E3 泛素连接酶 Smurf1 的 SUMO 化,损害成骨分化和创伤性异位骨化。
Biochim Biophys Acta Mol Cell Res. 2024 Oct;1871(7):119771. doi: 10.1016/j.bbamcr.2024.119771. Epub 2024 Jun 5.
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弥漫性肺骨化及其在特发性和继发性形式中与瘢痕性机化性肺炎的关联。
Sci Rep. 2025 Apr 11;15(1):12442. doi: 10.1038/s41598-025-95307-0.
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PROCR 成纤维细胞来源的钙化凋亡小体启动异位骨化。
J Extracell Vesicles. 2024 Apr;13(4):e12425. doi: 10.1002/jev2.12425.
4
Charting the cellular biogeography in colitis reveals fibroblast trajectories and coordinated spatial remodeling.绘制结肠炎中的细胞生物地理学揭示了成纤维细胞轨迹和协调的空间重塑。
Cell. 2024 Apr 11;187(8):2010-2028.e30. doi: 10.1016/j.cell.2024.03.013. Epub 2024 Apr 2.
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