摘要
心肌细胞中,p300是维持其分化表型所必须的转录辅激活因子。在心脏压力负荷增加等病理条件下,一些肥厚反应转录因子,如锌指蛋白GATA-4和肌细胞增强因子2(MEF2)等,可与p300相互作用,参与心肌细胞肥厚的病理过程。拮抗p300可有效阻断心肌肥厚的病理进程,进而改善心功能。更好地了解p300在心肌肥厚中的作用,对于未来治疗心肌肥厚和心力衰竭具有重要意义。
The transcriptional coactivator p300 functions as histone acetyltrasferase that regulates transcription via chromatin remodeling and is important in the processes of cell proliferation and differentiation in cardiac myocytes.p300 was involved in the pathological process of cardiac hypertrophy and was thought to be involved in cardiac myocyte growth through myocyte enhancer factor 2（MEF2）and GATA-4dependent transcription. The concept of inhibiting p300 histone acetyltransferase（HAT）is to blunt hypertrophy and reduce the rate of decompensation in the heart failure. Understanding precise mechanisms of p300 in the cardiac hypertrophy will highlight the importance of monitoring the cardiovascular impact of drugs that potentiate p300 activity on molecular pathways for hypertrophy and the heart failure.
出处
《中华高血压杂志》
CAS
CSCD
北大核心
2014年第12期1102-1107,共6页
Chinese Journal of Hypertension
