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在代谢应激下,SGLT2抑制通过SAM依赖的炎症基因表观遗传抑制来保护功能

Hiroshi Maekawa^1,2, Yalu Zhou^1,2, Yuki Aoi^3,4

¹Feinberg Cardiovascular & Renal Research Institute.

The Journal of clinical investigation

|October 1, 2025

概括

通过-葡萄糖携带载体2 (SGLT2) 抑制剂阻断脏葡萄糖再吸收,可以保护脏. 在SGLT2缺陷脏中增加的S-adenosylmethionine (SAM) 在表观遗传学上抑制炎症基因,提供脏保护.

科学领域:

腎臟病學 (nephrology) 是一種醫學專業.
代谢途径代谢途径
表观遗传学在表观遗传学中,表观遗传学是指表观遗传学.

背景情况:

-葡萄糖共运输体2 (SGLT2) 抑制剂减缓病的进展,但机制尚不清楚.
改变的代谢物可能解释SGLT2抑制所观察到的脏保护.
研究S-adenosylmethionine (SAM) 在SGLT2介导的保护中的作用.

研究的目的:

研究S-adenosylmethionine (SAM) 在与SGLT2功能丧失相关的保护中的作用.
阐明SGLT2抑制影响代谢物和炎症通路的机制.

主要方法:

在缺乏SGLT2功能的小鼠中,与高脂肪饮食中的野生型小鼠进行代谢物的比较.
评估功能和NF-κB通路基因的表达.
在近端管状细胞中对Mat2a/MAT2A表达的分析以及MAT2A抑制对脏保护的影响.

主要成果:

来自SGLT2缺乏小鼠的脏显示S-adenosylmethionine (SAM) 水平增加.
升高的SAM与改善功能和减少NF-κB通路基因表达相关.
观察到MAT2A抑制取消了脏的保护,并增加了NF-κB基因的H3K27三甲基化.

结论:

失去SGLT2会增加脏SAM水平,从而有助于脏的保护.
SAM通过基因组甲基化促进炎症基因的表观遗传抑制.
这项研究揭示了一种新的SGLT2介导脏保护机制,涉及SAM和表观遗传调节.

关键词:

糖尿病糖尿病糖尿病表观遗传学在表观遗传学中,表观遗传学是指表观遗传学.代谢过程中的代谢.在 NF-kappaBB 里.腎臟病學 (nephrology) 是一種醫學專業.

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