Increasing Mononuclear Diploid Cardiomyocytes by Loss of E2F Transcription Factor 7/8 Fails to Improve Cardiac Regeneration After Infarct.
Increasing Mononuclear Diploid Cardiomyocytes by Loss of E2F Transcription Factor 7/8 Fails to Improve Cardiac Regeneration After Infarct.
复制标题
通过 E2F 转录因子 7/8 的缺失来增加单核二倍体心肌细胞无法改善梗塞后的心脏再生。
DOI:
10.1161/circulationaha.122.061018
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发表时间:
2023
期刊:
影响因子:
37.8
通讯作者:
Evans,SylviaM
中科院分区:
文献类型:
--
作者:
Yu,Zhe;Zhang,Lunfeng;Cattaneo,Paola;Guimarães-Camboa,Nuno;Fang,Xi;Gu,Yusu;Peterson,KirkL;Bogomolovas,Julius;Cuitino,Cecilia;Leone,GustavoW;Chen,Ju;Evans,SylviaM
Transition of cardiomyocytes (CMs) from hyperplasic to hypertrophic growth occurs after birth, accompanied by binucleation and polyploidization, suggested as a barrier to cardiac regeneration. Cardiac regeneration and functional recovery after myocardial infarction (MI) have been correlated with an increased baseline frequency of mononuclear diploid (MND) CMs. 1 However, the capacity of MND adult CMs to undergo proliferation is still controversial. RNA-sequencing analyses of fluorescence-activated cell sorting–separated CMs suggested transcriptional differences between mononuclear and binuclear CMs, 2 yet other studies using scRNA-sequencing3 or bulk RNA-sequencing4 analyses found similar transcriptomes between mononuclear and multinuclear CMs in both normal and postinjury conditions. Our aim was to further investigate the regenerative potential of MND CMs.