| Literature DB >> 33833125 |
Masahito Ogawa1,2, Fan-Suo Geng3,4, David T Humphreys4,5, Esther Kristianto6, Delicia Z Sheng1, Subhra P Hui1, Yuxi Zhang7, Kotaro Sugimoto1, Maki Nakayama1, Dawei Zheng1, Daniel Hesselson4,7,8,9, Mark P Hodson6,10, Ozren Bogdanovic3,11, Kazu Kikuchi12,2,4.
Abstract
Cardiac regeneration requires dedifferentiation and proliferation of mature cardiomyocytes, but the mechanisms underlying this plasticity remain unclear. Here, we identify a potent cardiomyogenic role for Krüppel-like factor 1 (Klf1/Eklf), which is induced in adult zebrafish myocardium upon injury. Myocardial inhibition of Klf1 function does not affect heart development, but it severely impairs regeneration. Transient Klf1 activation is sufficient to expand mature myocardium in uninjured hearts. Klf1 directs epigenetic reprogramming of the cardiac transcription factor network, permitting coordinated cardiomyocyte dedifferentiation and proliferation. Myocardial expansion is supported by Klf1-induced rewiring of mitochondrial metabolism from oxidative respiration to anabolic pathways. Our findings establish Klf1 as a core transcriptional regulator of cardiomyocyte renewal in adult zebrafish hearts.Entities:
Year: 2021 PMID: 33833125 DOI: 10.1126/science.abe2762
Source DB: PubMed Journal: Science ISSN: 0036-8075 Impact factor: 47.728