通过其细胞内和细胞外的作用,PFKFB3促进肌纤维细胞分化和心脏纤维化
Bing Han1, Zhaowei Zhu2, Yongxiang Wang1
1Department of Cardiology, The First Hospital of Lanzhou University, No.1, Dong Gang West Road, Lanzhou, Gansu, 730000, China.
Journal of cardiovascular translational research
|October 30, 2025
概括
PFKFB3通过促进肌纤维细胞中的糖解和细胞外信号传递来增强心脏纤维化. 抑制PFKFB3可降低纤维化和肌纤维细胞活性,为心脏病提供潜在的治疗点.
科学领域:
- 心血管生物学 心血管生物学
- 代谢调节 代谢调节 代谢调节 代谢调节
- 纤维化研究 纤维化研究
背景情况:
- 心脏纤维化是一个重要的临床问题,治疗方法很少.
- 在心脏纤维化中,6-果糖-2-激酶/果糖-2,6-双酸酶3 (PFKFB3) 的特定作用尚不清楚.
研究的目的:
- 调查PFKFB3在心脏纤维化病原发生中的作用.
- 探索PFKFB3作为心肌病的潜在治疗点.
主要方法:
- 单细胞RNA测序用于分析心肌病中的基因表达.
- 西方斑块用于评估纤维化心脏和肌纤维细胞中的PFKFB3表达.
- 在心脏纤维化小鼠模型中,PFKFB3的遗传和药理抑制.
- 通过ELISA测量患者的血PFKFB3水平.
主要成果:
- 在心肌病中,激活的心脏肌纤维细胞 (myoCFs) 中,糖解显著增强.
- 在纤维化心脏和TGF-β1刺激的肌细胞中,PFKFB3的表达增加.
- 抑制PFKFB3可以减少肌细胞细胞的激活,增殖,迁移和心脏纤维化.
- 细胞外PFKFB3促进纤维细胞激活和炎症.
- 血PFKFB3水平升高与患者纤维化严重程度相关.
结论:
- PFKFB3在心脏纤维化中起着双重作用,通过糖解作用于细胞内和细胞外.
- 抑制PFKFB3是一种对心脏纤维化有前途的治疗策略.
- PFKFB3是心肌病中纤维化严重程度的潜在生物标志物.
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