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Updated: Jan 31, 2026

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高血糖诱导的P300/CBP乙转移酶驱动ZEB2介导的炎症性巨细胞,并延迟伤口愈合
Soumyajit Roy1, Debarun Patra2, Palla Ramprasad1
1Department of Biomedical Engineering, Indian Institute of Technology Ropar, Rupnagar, India.
JCI insight
|January 29, 2026
概括
持续的高血糖症会提高伤口巨细胞中的ZEB2表达,促进炎症和延迟愈合. 抑制P300减少ZEB2,缓解炎症并加速糖尿病伤口的修复.
科学领域:
- 生物医学科学 生物医学科学
- 分子生物学分子生物学
- 免疫学 免疫学 免疫学
背景情况:
- 慢性高血糖症通过改变细胞功能来损害伤口愈合.
- 在糖尿病伤口愈合期间巨细胞极化中ZEB2 (指E-box结合 homeobox 2) 的作用尚不清楚.
研究的目的:
- 调查ZEB2在巨细胞极化和糖尿病伤口愈合中的炎症中的作用.
- 探索P300/CBP作为改善高血糖症中伤口修复的治疗标.
主要方法:
- 在高血糖条件下的伤口巨细胞中检查了ZEB2表达.
- 研究了ZEB2操纵 (强迫表达和沉默) 对巨细胞两极分化的影响.
- 在糖尿病伤口愈合的小鼠模型中利用C646,一种P300抑制剂.
主要成果:
- 过高血糖症通过P300/CBP介导的素乙化增加了伤口巨细胞中ZEB2的表达.
- 强迫ZEB2表达促进了亲炎性巨细胞表型.
- 在糖尿病小鼠中,沉默ZEB2降低了炎症并改善了伤口愈合.
- 用C646抑制P300降低了ZEB2,减少了炎症,并加速了伤口愈合.
结论:
- 由高血糖引起的ZEB2上调有助于慢性炎症和延迟伤口愈合.
- 针对P300抑制ZEB2为糖尿病伤口并发症提供了潜在的治疗策略.
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