OGFOD1 modulates the transcriptional and proteomic landscapes to alter isoproterenol-induced hypertrophy susceptibility

被引：2
|
作者：
Rodriguez, Rebeca [1 ]
Harris, Michael [1 ]
Murphy, Elizabeth [1 ]
Kennedy, Leslie M. [1 ,2 ]
机构：
[1] NHLBI, Cardiovasc Branch, NIH, Bethesda, MD USA
[2] Bldg 10,Rm 6N248,10 Ctr Dr, Bethesda, MD 20892 USA
来源：
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY | 2023年 / 179卷
关键词：
Heart failure; Cardiac hypertrophy; Translation; Post-translational modifications; Proline hydroxylation; CARDIAC-HYPERTROPHY; TRANSLATION;
D O I：
10.1016/j.yjmcc.2023.04.002
中图分类号：
R5 [内科学];
学科分类号：
1002 ; 100201 ;
摘要：
Cardiac hypertrophy is associated with increased translation. However, little is known of the mechanisms that regulate translation in hypertrophy. Members of the 2-oxoglutarate-dependent dioxygenase family regulate several aspects of gene expression, including translation. An important member of this family is OGFOD1. Here, we show OGFOD1 accumulates in failing human hearts. Upon OGFOD1 deletion, murine hearts showed transcriptomic and proteomic changes, with only 21 proteins and mRNAs (0.6%) changing in the same direction. Additionally, OGFOD1-KO mice were protected from induced hypertrophy, supporting a role for OGFOD1 in the cardiac response to chronic stress.
引用
收藏
页码：42 / 46
页数：5
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