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铁依赖的KDM4D活动通过PI3K-Akt-Foxo1通路控制MSC的静止活动平衡

Zhongyu Xie¹, Yunshu Che^1,2, Guo Huang³

¹Department of Orthopedics, The Eighth Affiliated Hospital, Sun Yat-sen University, Shenzhen, 518033, P. R. China.

Cellular and molecular life sciences : CMLS

|August 19, 2024

概括

缺铁会通过降低KDM4D脱甲基酶活性,影响骨代谢,损害中干细胞的激活. 恢复PI3K-Akt-Foxo1通路可以逆转与缺铁相关的骨损失.

科学领域:

生物化学生物化学
细胞生物学细胞生物学
骨的新陈代谢骨的新陈代谢

背景情况:

缺铁是一种广泛的营养问题,影响器官功能.
新出现的证据将铁缺乏与骨代谢功能障碍联系起来,但机制尚不清楚.
铁依赖酶调节细胞过程,但它们在铁缺乏下中酶干细胞 (MSC) 激活中的作用尚不清楚.

研究的目的:

调查质脱甲基酶活性在缺铁诱导的静止MSC激活抑制中的作用.
确定参与这个过程的关键分子参与者.

主要方法:

研究KDM4D在铁缺乏症下MSC激活中的作用.
评估了H3K9me3脱甲基酶活性和PIK3R3促进体附近的异染色体形成.
利用缺铁的小鼠模型来评估骨髓MSC激活和骨质.
研究了PI3K-Akt-Foxo1通路的参与.

主要成果:

确定KDM4D对于静止MSC激活至关重要.
缺铁严重降低了KDM4D的H3K9me3脱甲基酶活性.
在PIK3R3促进体附近增加的异色染色素通过PI3K-Akt-Foxo1通路抑制了其表达,抑制了MSC激活.
缺铁的小鼠显示MSC激活受损,骨质减少.

结论:

缺铁会通过降低KDM4D活性来抑制MSC激活,从而导致PIK3R3的下调和PI3K-Akt-Foxo1通路的破坏.
这种机制有助于铁缺乏的骨质损失.
向PI3K-Akt-Foxo1通路为铁缺乏引起的骨损失提供了潜在的治疗策略.

关键词:

H3K9me3是什么意思 H3K9me3是什么意思铁缺乏症铁缺乏症这就是KDM4D.多国中心的MSCs.骨质疏松症是一种骨质疏松症.静止是一种静止.

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