對心臟衰竭患者使用干細胞療法所存在的障礙包括：難以確保心臟祖細胞分化成功能性心室心肌細胞,，以及難以確保能將分化的細胞輸送和集成到患者的“心室肌”中,。Neil Chi及其同事研究了特定心肌細胞類型在斑馬魚胚胎心臟中分化成密切相關(guān)的、但卻截然不同的細胞類型的能力,。他們發(fā)現(xiàn),，分化的心房心肌細胞在心臟受傷時能轉(zhuǎn)變成心室心肌細胞，而且Notch信號作用通道誘導這種再生,。這項研究將內(nèi)源性心臟細胞類群確定為心室再生的一個潛在來源,。（生物谷Bioon.com）
生物谷推薦英文摘要：
Nature doi:10.1038/nature12322
In vivo cardiac reprogramming contributes to zebrafish heart regeneration
Ruilin Zhang,Peidong Han,Hongbo Yang,Kunfu Ouyang,Derek Lee,Yi-Fan Lin,Karen Ocorr,Guson Kang,Ju Chen,Didier Y. R. Stainier,Deborah Yelon& Neil C. Chi
Despite current treatment regimens, heart failure remains the leading cause of morbidity and mortality in the developed world due to the limited capacity of adult mammalian ventricular cardiomyocytes to divide and replace ventricular myocardium lost from ischaemia-induced infarct. Hence there is great interest to identify potential cellular sources and strategies to generate new ventricular myocardium. Past studies have shown that fish and amphibians and early postnatal mammalian ventricular cardiomyocytes can proliferate to help regenerate injured ventricles; however, recent studies have suggested that additional endogenous cellular sources may contribute to this overall ventricular regeneration. Here we have developed, in the zebrafish (Danio rerio), a combination of fluorescent reporter transgenes, genetic fate-mapping strategies and a ventricle-specific genetic ablation system to discover that differentiated atrial cardiomyocytes can transdifferentiate into ventricular cardiomyocytes to contribute to zebrafish cardiac ventricular regeneration. Using in vivo time-lapse and confocal imaging, we monitored the dynamic cellular events during atrial-to-ventricular cardiomyocyte transdifferentiation to define intermediate cardiac reprogramming stages. We observed that Notch signalling becomes activated in the atrial endocardium following ventricular ablation, and discovered that inhibiting Notch signalling blocked the atrial-to-ventricular transdifferentiation and cardiac regeneration. Overall, these studies not only provide evidence for the plasticity of cardiac lineages during myocardial injury, but more importantly reveal an abundant new potential cardiac resident cellular source for cardiac ventricular regeneration.
