| First Author | Zhou Z | Year | 2017 |
| Journal | Cell Rep | Volume | 18 |
| Issue | 4 | Pages | 1019-1032 |
| PubMed ID | 28122228 | Mgi Jnum | J:254721 |
| Mgi Id | MGI:6103797 | Doi | 10.1016/j.celrep.2017.01.002 |
| Citation | Zhou Z, et al. (2017) Temporally Distinct Six2-Positive Second Heart Field Progenitors Regulate Mammalian Heart Development and Disease. Cell Rep 18(4):1019-1032 |
| abstractText | The embryonic process of forming a complex structure such as the heart remains poorly understood. Here, we show that Six2 marks a dynamic subset of second heart field progenitors. Six2-positive (Six2(+)) progenitors are rapidly recruited and assigned, and their descendants are allocated successively to regions of the heart from the right ventricle (RV) to the pulmonary trunk. Global ablation of Six2(+) progenitors resulted in RV hypoplasia and pulmonary atresia. An early stage-specific ablation of a small subset of Six2(+) progenitors did not cause any apparent structural defect at birth but rather resulted in adult-onset cardiac hypertrophy and dysfunction. Furthermore, Six2 expression depends in part on Shh signaling, and Shh deletion resulted in severe deficiency of Six2(+) progenitors. Collectively, these findings unveil the chronological features of cardiogenesis, in which the mammalian heart is built sequentially by temporally distinct populations of cardiac progenitors, and provide insights into late-onset congenital heart disease. |
