Developmental and Stem Cell Biology Division, Victor Chang Cardiac Research Institute, Darlinghurst, New South Wales, Australia.
Department of Regenerative Medicine and Tissue Engineering, National Cerebral and Cardiovascular Center Research Institute, Suita, Osaka, Japan.
Science. 2021 Apr 9;372(6538):201-205. doi: 10.1126/science.abe2762.
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.
心脏再生需要成熟心肌细胞的去分化和增殖,但这种可塑性的机制仍不清楚。在这里,我们发现了 Krüppel 样因子 1(Klf1/Eklf)在成体斑马鱼心肌损伤后的心肌中有很强的心肌发生作用。心肌中 Klf1 功能的抑制不会影响心脏发育,但会严重损害再生。瞬时 Klf1 激活足以扩张未受伤心脏中的成熟心肌。Klf1 指导心脏转录因子网络的表观遗传重编程,允许协调的心肌细胞去分化和增殖。Klf1 诱导的线粒体代谢从氧化呼吸到合成代谢途径的重新布线为心肌扩张提供了支持。我们的研究结果确立了 Klf1 作为成年斑马鱼心脏中心肌细胞更新的核心转录调节因子。