脂肪质量和与肥胖相关的 (FTO) /SOCS6-m6轴表观遗传修饰通过调节角质细胞功能来将肥胖与亚托皮炎联系起来
Fugang Xiao1, Ruoya Wu1, Ningling Wu1
1Department of Dermatology, The Third Xiangya Hospital, Central South University, Changsha, Hunan Province, 410013, P. R. China.
The Journal of investigative dermatology
|February 5, 2026
概括
肥胖会对皮肤细胞中的FTO酶进行上调,通过减少SOCS6蛋白来导致亚托皮炎 (AD). 准这一FTO/SOCS6-m6途径可能治疗与肥胖相关的AD.
科学领域:
- 分子生物学分子生物学
- 免疫学 免疫学 免疫学
- 皮肤病学 皮肤病学
背景情况:
- 亚托邦性皮肤炎 (AD) 涉及皮肤屏障缺陷和免疫问题.
- 肥胖与阿尔茨海默病有关,但分子联系,特别是RNA代谢,尚不清楚.
研究的目的:
- 研究与肥胖相关的RNA代谢变化如何驱动AD.
- 确定肥胖-AD连接中的关键分子参与者.
主要方法:
- 集成的转录和表转录测序.
- 在角质细胞 (KCs) 中分析FTO目标.
- 在体内局部FTO敲击模型.
主要成果:
- 肥胖增加了病变表皮KC中的FTO,导致AD.
- FTO针对SOCS6mRNA,通过m6A脱甲基化降低其稳定性和蛋白质.
- 这种FTO/SOCS6轴激活了KC的炎症通路 (IL-1β,S100A8/A9),使AD恶化.
结论:
- FTO/SOCS6-m6表观遗传轴是肥胖和AD之间的关键联系.
- 在AD病理学中FTO的作用是因果关系的.
- FTO和SOCS6是精确AD管理的潜在治疗目标.
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