CTRP9通过抑制内皮细胞向间质转化改善糖尿病诱导的心脏纤维化

李威; 贺立群; 张帆

doi:10.14188/j.1671-8852.2025.0956

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CTRP9通过抑制内皮细胞向间质转化改善糖尿病诱导的心脏纤维化

基础医学研究 | 更新时间：2026-11-05

- CTRP9通过抑制内皮细胞向间质转化改善糖尿病诱导的心脏纤维化
- CTRP9 improves diabetes‑induced cardiac fibrosis by inhibiting endothelial⁃to⁃mesenchymal transition
- 武汉大学学报（医学版） 2025年46卷第11期页码：1381-1387
- 作者机构：
  
  武汉市第一医院心内科湖北武汉 430022
- 作者简介：
  
  李威，男，1992—，医学硕士，主要从事冠心病的发生发展及机制研究，E‑mail:8869363054@qq.com
  张帆，男，1978—，医学硕士，副主任医师，主要从事心血管疾病的研究，E‑mail:13720277068@126.com
- 基金信息：
  
  湖北省卫生健康委科研项目(WJ2023F043)
- DOI：10.14188/j.1671-8852.2025.0956
  中图分类号： R541.4
- 收稿：2025-08-20，
  
  纸质出版：2025-11-25
- 稿件说明：
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李威,贺立群,张帆.CTRP9通过抑制内皮细胞向间质转化改善糖尿病诱导的心脏纤维化[J].武汉大学学报（医学版）,2025,46(11):1381-1387.

LI Wei,HE Liqun,ZHANG Fan.CTRP9 improves diabetes‑induced cardiac fibrosis by inhibiting endothelial⁃to⁃mesenchymal transition[J].Medical Journal of Wuhan University,2025,46(11):1381-1387.
李威,贺立群,张帆.CTRP9通过抑制内皮细胞向间质转化改善糖尿病诱导的心脏纤维化[J].武汉大学学报（医学版）,2025,46(11):1381-1387. DOI： 10.14188/j.1671-8852.2025.0956.

LI Wei,HE Liqun,ZHANG Fan.CTRP9 improves diabetes‑induced cardiac fibrosis by inhibiting endothelial⁃to⁃mesenchymal transition[J].Medical Journal of Wuhan University,2025,46(11):1381-1387. DOI： 10.14188/j.1671-8852.2025.0956.

摘要

目的

研究C1q/肿瘤坏死因子相关蛋白‑9（CTRP9）在糖尿病诱导的内皮‑间质转化（EndMT）中的潜在作用和机制。

方法

将实验小鼠随机分为4组（Control、DM、Ad‑GFP+DM、Ad‑CTRP9+DM），在相应组16周龄小鼠尾静脉注射Ad‑CTRP9（1×10

pfu）或Ad‑GFP（1×10

pfu），首次腺病毒注射4周后进行心脏超声检测，在20周龄时麻醉处死小鼠，获取小鼠心脏组织、Masson染色、免疫组化染色。通过蛋白印迹法（Western Blot）、定量实时PCR（RT‑PCR）检测EndMT相关标志物（CD31、α‑SMA、FSP1、Collagen Ⅰ、Collagen Ⅲ、TGF‑β1、CTGF）。

结果

糖尿病小鼠血浆中CTRP9表达水平有所下降，高血糖促进EndMT的进展并加重了体内胶原沉积，而CTRP9过表达后能改善这一过程，且不影响糖尿病小鼠的心脏功能。

结论

CTRP9能减轻糖尿病诱导的EndMT。

Abstract

Objective

To investigate the potential role and mechanism of C1q/tumor necrosis factor‑related protein‑9 (CTRP9) in diabetes‑induced endothelial‑mesenchymal transition (EndMT).

Methods

The experimental mice were randomly divided into four groups (Control

Ad‑GFP+DM

and Ad‑CTRP9+DM). At 16 weeks of age

the mice were injected with Ad‑CTRP9 (1×10

pfu) or Ad‑GFP (1×10

pfu) via the tail vein. Four weeks after the first adenovirus injection

a cardiac ultrasound was performed. Then

the mice were anesthetized and sacrificed at the age of 20 weeks. The heart tissues were obtained for Masson staining and immunohistochemical staining. The EndMT‑related markers (CD31

α‑SMA

FSP1

Collagen Ⅰ

Collagen Ⅲ

TGF‑β1

and CTGF) were detected by Western Blot and quantitative real‑time PCR (RT‑PCR).

Results

The plasma level of CTRP9 was decreased in diabetic mice. Hyperglycemia prom

oted endothelial⁃to⁃mesenchymal transition (EndMT) and exacerbated collagen deposition

in vivo

whereas CTRP9 overexpression attenuated these effects without influencing cardiac function in diabetic mice.

Conclusion

The CTRP9 can alleviate diabetes‑induced EndMT.

关键词

Keywords

references

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