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心脏衰老是由伪阴极症促进的增加p300诱导的糖解

Simone Serio^1,2, Christina Pagiatakis^1,3, Elettra Musolino³

¹Department of Cardiovascular Medicine, IRCCS Humanitas Research Hospital, via Manzoni 56, 20089 Rozzano (MI), Italy (S.S., C.P., A.F., P.C., J.L.F., L.P., G.R., N.S., M.M., G.C., R.P.).

Circulation research

|September 8, 2023

概括

老化的心脏由于代谢重塑而增加了葡萄糖分解. 抑制p300/CBP联合激活剂可以逆转这种情况,改善心脏功能,并建议心力衰竭治疗的目标.

科学领域:

心脏病学心脏病学
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.

背景情况:

心力衰竭在老年人中很常见.
衰老会导致心脏细胞的代谢变化,增加葡萄糖分解和减少能量生产,导致功能衰退.
了解这些代谢变化是治疗与年龄有关的心脏功能障碍的关键.

研究的目的:

探索三种组素修饰 (H3K27ac,H3K27me3,H3K4me1) 在与年龄相关的心脏代谢重塑中的作用.
为了研究转录协激活剂p300/CBP在心脏衰老中的功能.

主要方法:

对不同年龄小鼠的表观基因组,转录基因组和代谢基因组数据进行交叉比较.
利用p300/CBP基因组乙转移酶的特定抑制剂来评估其在心脏衰老中的作用.

主要成果:

确定了与衰老心肌细胞的转录变化相关的保存增强剂.
在老老鼠心脏中观察到P300/CBP的活性增加,通过伪氧促进糖解.
抑制p300/CBP预衰老导致更有氧的新陈代谢,增强收缩性,并减轻心脏衰退.

结论:

葡萄糖溶解增强剂的表观遗传调节与与年龄有关的心力衰竭有关.
针对糖溶解通路的表观遗传失调,为老年心力衰竭患者提供了潜在的治疗策略.

关键词:

这是一种CREB结合蛋白.老化的老化衰老的老化心脏衰竭是因为心脏衰竭.人类人类人类人类人类人类.鼠标鼠标鼠标鼠标

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