Glucocorticoids accelerate fibrosis in steroid-induced osteonecrosis of the femoral head by inducing paracrine pro-fibrotic factors from vascular endothelial cells

JIN Runze; ZHU Weiwen; LI Bingfei; LU Xingchen; LIU Xi; GONG Zhiwei; ZHANG Xiaoqi; ZHANG Zhaoyuan; LIU Kesi; CHEN Lifeng; ZHANG Wei; BAI Chuanqing; NI Zhenhong; ZHOU Lan; XIONG Yan

doi:10.16016/j.2097-0927.202602073

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Glucocorticoids accelerate fibrosis in steroid-induced osteonecrosis of the femoral head by inducing paracrine pro-fibrotic factors from vascular endothelial cells

Monographic Reports | 更新时间：2026-06-30

- Glucocorticoids accelerate fibrosis in steroid-induced osteonecrosis of the femoral head by inducing paracrine pro-fibrotic factors from vascular endothelial cells
- Journal of Army Medical University Vol. 48, Issue 12, Pages: 1667-1678(2026)
- 作者机构：
  
  1.陆军军医大学（第三军医大学）大坪医院：，骨科，重庆
  2.陆军军医大学（第三军医大学）大坪医院：，康复医学科，重庆
  3.联勤保障部队第九八八医院耳鼻喉科与颌面外科，河南郑州
  4.重庆医药高等专科学校附属第一医院急危重症医学部，重庆
- 作者简介：
  
  ZHOU LanE-mail： zhou930@163.com
  XIONG YanE-mail： xiongyandoctor@tmmu.edu.cn
- 基金信息：
  
  the Science Fund for Distinguished Young Scholars of Chongqing(CSTB2024NSCQ-JQX0019);the Special Project of Science and Technology Innovation Capacity Promotion of Army Medical University(2023XQN44)
- DOI：10.16016/j.2097-0927.202602073
  CLC： R347.7;R363.21;R681.8
- Received：13 February 2026，
  
  Revised：2026-04-01，
  
  Published：30 June 2026
- 稿件说明：
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靳润泽，朱卫文，李冰飞，等.糖皮质激素通过诱导血管内皮细胞旁分泌促纤维化因子加速激素性股骨头坏死纤维化［J］.陆军军医大学学报，2026，48（12）：1667-1678.DOI：10.16016/j.2097-0927.202602073.

JIN R Z，ZHU W W，LI B F，et al.Glucocorticoids accelerate fibrosis in steroid-induced osteonecrosis of the femoral head by inducing paracrine pro-fibrotic factors from vascular endothelial cells［J］.J Army Med Univ，2026，48（12）：1667-1678.DOI：10.16016/j.2097-0927.202602073.
靳润泽，朱卫文，李冰飞，等.糖皮质激素通过诱导血管内皮细胞旁分泌促纤维化因子加速激素性股骨头坏死纤维化［J］.陆军军医大学学报，2026，48（12）：1667-1678.DOI：10.16016/j.2097-0927.202602073. DOI：

JIN R Z，ZHU W W，LI B F，et al.Glucocorticoids accelerate fibrosis in steroid-induced osteonecrosis of the femoral head by inducing paracrine pro-fibrotic factors from vascular endothelial cells［J］.J Army Med Univ，2026，48（12）：1667-1678.DOI：10.16016/j.2097-0927.202602073. DOI：

摘要

目的

探究激素性股骨头坏死（glucocorticoid-induced osteonecrosis of the femoral head，GONFH）模型中，损伤的血管内皮细胞对股骨头坏死区域纤维化进程的调控作用，并深入解析其潜在分子机制，为GONFH的纤维化干预及临床治疗提供理论依据。

方法

①临床样本组织学检测：随机选取2023年12月至2025年12月期间大坪医院骨科收治的5例确诊为GONFH患者的股骨头样本作为试验组，同时选取5例因股骨颈骨折（femoral neck fracture，FNF）行手术治疗患者的股骨头样本作为正常对照组。对坏死反应带进行石蜡切片，HE染色、天狼星红染色、α-SMA/FN的Western blotting及CD31免疫荧光染色，评估组织形态、胶原沉积、纤维化相关蛋白表达及血管内皮细胞分布。②体外细胞实验：明确地塞米松（dexamethasone，DEX）处理后人脐静脉血管内皮细胞（human umbilical vein endothelial cell，HUVEC）分泌的因子对肌成纤维细胞活化的影响。应用转化生长因子-β（transforming growth factor-beta，TGF-β）诱导人骨髓间充质干细胞（human bone marrow mesenchymal stem cells，hBMSC）分化为肌成纤维细胞，成功后将HUVEC分为DEX处理组（作用48 h）和PBS对照组，收集2组细胞的条件培养基（conditioned medium，CM），将CM-DEX组和CM-PBS组分别与肌成纤维细胞共孵育48 h，Western blot检测肌成纤维细胞中α-SMA、Ⅰ型胶原蛋白（collagen type，Col Ⅰ）及FN的蛋白表达水平。③分子机制探究：提取CM-DEX组与CM-PBS组HUVEC总RNA，RNA转录组测序（RNA-seq），筛选两组间差异表达基因（DEGs），行GO功能富集和KEGG通路富集分析。收集2组HUVEC分泌蛋白行蛋白组学测序，筛选差异分泌蛋白，结合生物信息学分析其通路及与肌成纤维细胞活化的关联。

结果

①临床样本检测结果：与FNF对照组相比，GONFH组股骨头反应带区域：HE染色示组织排列紊乱、纤维组织增生；天狼星红染色示胶原沉积显著增加（

0.000 1）；α-SMA（

0.01）及FN（

0.000 1）蛋白表达升高。CD31⁺血管内皮细胞数量增多（

0.000 1）且形成管状结构；α-SMA肌成纤维细胞数量增加（

0.000 1），且与CD31细胞空间分布邻近。②体外细胞实验结果：与CM-PBS组比较，CM-DEX组肌成纤维细胞中α-SMA（

0.01）及FN（

0.01）蛋白表达升高，ColⅠ表达无显著差异（

=0.131 0）。③分子测序：RNA-seq显示，CM-DEX组HUVEC上调620个基因，筛选出30个促纤维化/炎症相关基因，前5位为

PTPRN2

、

TSC22D3

、

FKBP5

、

MAFB

、

SYP

。GO富集于蛋白结合、转录调控、蛋白转运等；KEGG富集于TGF-β、JAK-STAT、MAPK、SNARE囊泡运输及外泌体通路。蛋白组学显示，CM-DEX组HUVEC分泌20个促纤维化相关蛋白（如TGFBR1、SMAD2、RAB11B、DCN等）。GO富集于细胞外基质、胶原相关功能；KEGG富集于补体与凝血级联、细胞外基质（extracellular matrix，ECM）-受体互作、黏着斑等通路。

结论

糖皮质激素可诱导血管内皮细胞异常活化，通过TGF-β、PI3K-Akt及囊泡运输/外泌体等通路，促进DCN、RAB11B、TGFBR1等促纤维化因子高表达；这些因子旁分泌作用于成纤维细胞，促使其活化并过度合成ECM（Col Ⅰ、FN）。GONFH患者股骨头反应带中血管内皮细胞增多且与肌成纤维细胞空间邻近，进一步加剧纤维化进程。

Abstract

Objective

To investigate the regulatory role of injured vascular endothelial cells in the fibrosis progression in the necrotic region of the femoral head in a glucocorticoid-induced osteonecrosis of the femoral head (GONFH)

and further elucidate the underlying molecular mechanisms

so as to provide a theoretical basis for anti-fibrotic intervention and clinical treatment of GONFH.

Methods

① Clinical sample histological examination: Femoral head samples were collected from 5 patients diagnosed with GONFH admitted to Department of Orthopedics of Daping Hospital between December 2023 and December 2025 and assigned to the experimental group. Meanwhile

femoral head specimens from 5 patients undergoing surgical treatment for

femoral neck fracture (FNF) were selected as the normal control group. Paraffin sections from the reactive zone of necrotic tissues were prepared. HE staining

Sirius red staining

Western blotting for α-smooth muscle actin (α-SMA) and fibronectin (FN)

and CD31 immunofluorescence staining were performed to evaluate tissue morphology

collagen deposition

expression of fibrosis-related proteins and distribution of vascular endothelial cells. ②

In vitro

experiments: The effect of factors secreted by dexamethasone (DEX)-treated human umbilical vein endothelial cells (HUVEC) on myofibroblast activation was determined. Human bone marrow mesenchymal stem cell (hBMSC) was induced to differentiate into myofibroblasts using transforming growth factor-β (TGF-β). HUVEC were then divided into a DEX treatment group (48 h) and a PBS control group

and conditioned medium (CM) was collected from both groups. CM-DEX and CM-PBS were co-incubated with myofibroblasts for 48 h

and Western blotting was applied to detect the protein expression levels of α-SMA

collagen type I (Col I)

and FN in myofibroblasts. ③ Exploration of molecular mechanisms: Total RNA was extracted from DEX-treated and control HUVEC for RNA sequencing (RNA-seq) to screen differentially expressed genes (DEGs) between the 2 groups. Gene Ontology (GO) functional enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were conducted. Secreted proteins from both groups of HUVEC were collected for proteomic sequencing

and differentially secreted proteins were screened. Bioinformatics analysis was used to analyze their pathways and association with myofibroblast activation.

Results

① Clinical sample findings: Compared with the FNF control group

the reactive zone of the femoral head in the GONFH group showed: disorganized tissue arrangement and fibrous hyperplasia by HE staining; markedly increased collagen deposition by Sirius red staining (

0.000 1); and elevate

d protein expression of α-SMA (

0.01) and FN (

0.000 1). The number of CD31 vascular endothelial cells was increased (

0.000 1) with evident formation of tubular structures

and the count of α-SMA myofibroblasts was also elevated (

0.000 1). In addition

α-SMA myofibroblasts were spatially adjacent to CD31

endothelial cells. ②

In vitro

experiment results: Compared with the CM-PBS group

the expression levels of α-SMA and FN were significantly increased in myofibroblasts of the CM-DEX group (both

0.01)

while no significant difference was observed in Col Ⅰexpression (

=0.131 0). ③Molecular sequencing: RNA-seq results revealed that 620 genes were upregulated in DEX-treated HUVECs

and 30 of them were identified as pro-fibrotic/inflammation-related. The top 5 genes were PTPRN2

TSC22D3

FKBP5

MAFB and SYP. GO enrichment analysis indicated that these genes were mainly involved in protein binding

transcriptional regulation and protein transport. KEGG enrichment analysis revealed enrichment in TGF-β

JAK-STAT

MAPK

SNARE vesicular transport and exosome pathways. Proteomic analysis identified 20 pro-fibrotic proteins secreted by DEX-treated HUVEC

including TGFBR1

SMAD2

RAB11B and DCN. GO terms were predominantly enriched in extracellular matrix (ECM) and collagen-related functions. KEGG pathways were mainly enriched in the complement and coagulation cascades

ECM-receptor interaction and focal adhesion pathways.

Conclusion

Glucocorticoids induce abnormal activation of vascular endothelial cells

which promotes high expression of pro-fibrotic factors such as DCN

RAB11B

and TGFBR1 through the TGF-β

PI3K-Akt

and vesicle transport/exosome pathways. These factors act on fibroblasts in a paracrine fashion

promote fibroblast activation and excessive synthesis of ECM components including Col Ⅰ and FN. In the reactive zone of the femoral head in GONFH patients

the increased number of vascular endothelial cells and their spatial proximity to myofibroblasts further exacerbate the fibrosis process.

关键词

Keywords

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