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在视网膜血管损伤和恢复中非典型的p38激酶信号

Lillian Schulz¹, Abby E Young¹, Fang Liu²

¹Department of Pharmaceutical and Biomedical Sciences, College of Pharmacy, University of Georgia, Athens, Georgia, USA.

FASEB journal : official publication of the Federation of American Societies for Experimental Biology

|December 13, 2025

概括

在小鼠中阻断非典型的p38信号减少了视网膜损伤和氧气诱导视网膜病变中的病态血管生长. 这表明血管视网膜病变的新治疗点.

科学领域:

眼科医生眼科眼科
分子生物学分子生物学
血管生物学血管生物学

背景情况:

血管视网膜病变影响全球数百万人,抗VEGF疗法提供有限的解决方案.
线原激活蛋白激酶 (MAPK) p38信号传递对于血管稳态和疾病至关重要,但在视网膜病变中,非典型的途径仍然未被探索.
不典型的p38信号传递,由TAB1介导,调节炎症和血管完整性.

研究的目的:

研究非典型的p38信号在氧气诱导视网膜病变 (OIR) 中的作用.
在OIR小鼠模型中探索抑制非典型p38信号的治疗潜力.

主要方法:

利用基因敲进小鼠模型 (Tab1^KI) 来阻止非典型的p38活动.
在Tab1^KI和野生型小鼠中诱导氧气诱导视网膜病变 (OIR).
进行了视网膜RNA测序 (RNAseq) 来分析转录变化.

主要成果:

与对照组相比,KI小鼠的血管消灭和新血管化显著减少.
抑制非典型的p38改变的转录特征,减少Mef2c信号传递.
降低Mef2c信号导致微质激活和炎症增加,但降低了病理血管生成,同时促进了生理血管再生.

结论:

选择性抑制非典型的p38信号有效地减少了OIR中的病理性新血管化,而不妨碍血管修复.
不典型的p38信号传递,通过Mef2c,在调节血管视网膜病变中的病态血管生成中起着关键作用.
准非典型的p38为治疗血管视网膜病变提供了一个有希望的新疗法策略.

关键词:

在 Tab1 Tab1 中.血管新生是因为血管新生.非典型的p3838 氧气诱导的视网膜病变是一种视网膜病变.视网膜视网膜视网膜是一个

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