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通过HIF诱导DEPP1 介导出缺血性心肌病的多种特征

Gregory A Wyant^1,2, Qinqin Jiang¹, Madhu Singh²

¹Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA (G.A.W., Q.J., C.L., W.G.K.).

|June 17, 2024

概括

心脏中低氧诱导因子 (HIF) 的激活会导致心脏功能障碍. 我们发现DEPP1通过促进线粒体和过氧体损失进行调解, 确定它是缺血性心肌病的治疗点.

科学领域:

心血管生物学
分子医学
细胞生理学

背景情况:

低氧诱导因子 (HIF) 极大地调节心脏功能.
心脏中的慢性HIF激活模仿了缺血性心肌病的特征,如线粒体损失和功能障碍.
导致心脏功能障碍的确切机制尚不清楚.

研究的目的:

阐明慢性HIF激活诱导心脏功能障碍的分子机制.
确定HIF诱导的心脏重塑和功能障碍的新媒介.

主要方法:

使用心脏特异性pVHL缺陷的小鼠来模型慢性HIF激活.
使用免疫染,RNA测序,自流量测定和活细胞成像.
应用CRISPR-Cas9基因编辑来验证体内关键分子参与者.

主要成果:

确定了一种新的途径,其中HIF诱导DEPP1 (由孕激素诱导的决定性蛋白质1).
DEPP1定位在线粒体中,对缺氧诱导的自和心肌细胞中的脂质积累至关重要.
缺少DEPP1可提高心肌细胞的存活率,并在体内减轻心脏功能障碍.

结论:

在慢性缺氧条件下,DEPP1是心脏重塑和功能障碍的关键媒介.
针对DEPP1是一种潜在的治疗策略,用于缺血性心肌病.

关键词:

在DEPP1 在HIF 在VHL 自食症心肌细胞没有氧气线粒体过氧体

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