NIH R01 · 2024
Integrating Transcriptome Reprogramming Into Cardiac Plasticity Regulatory Mechanisms
PROJECT SUMMARY Nearly every stressor reactivates the fetal gene program in cardiac myocytes, but why they make this transition is unclear given fetal metabolic and functional reprogramming is insufficient to sustain adult cardiac performance yet this fate change negatively impacts cardiac regeneration, which is an underlying determinant of heart failure. Thus, understanding fetal to adult myocyte state transitions is has broad therapeutic impact when considering how to boost the heart’s performance and tolerance for pathologic stress. A potent regulator of fetal to adult state transitions and the switch from hyperplastic to hypertrophic growth in the postnatal heart is an RNA binding…
From the public funding record at NIH RePORTER. Describes the funded project, not the reviews below.