During the first weeks after birth, cardiomyocytes within the mouse heart progressively exit the cell cycle, binucleate, and lose regenerative capacity.  We have determined that postnatal day 14 (P14) mouse hearts incapable of responding to thryoid hormone signaling have enhanced proliferation, retain greater populations of mononucleated cardiomyocytes, and show increased regenerative ability. In this study, we perform transcriptome-wide analysis to identify gene networks regulating thryoid hormone-dependent exit of cardiomyocyte cell-cycle and loss of regenerative potential. SOURCE: Guo,N,Huang (Guo.Huang@ucsf.edu) - Huang University of California, San Francisco

Pluto Bioinformatics

GSE125596: Transcriptome-wide profiling of thyroid hormone-dependent gene expression in the mouse heart