Mending broken hearts: cardiac development as a basis for adult heart regeneration and repair.
Mending broken hearts: cardiac development as a basis for adult heart regeneration and repair.
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DOI：
10.1038/nrm3619
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发表时间：
2013-08
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由于成年哺乳动物心脏再生和修复的潜力有限，心肌细胞在损伤和疾病期间的损失可导致心力衰竭和死亡。心脏生长和发育中涉及的细胞过程和调节机制可以被利用来通过在胚胎发生期间活跃的“重新唤醒”途径来修复受损的成年心脏。啮齿类动物的心脏功能已经通过将非肌细胞重编程为心肌细胞，通过表达控制心肌细胞身份的转录因子（GATA 4、HAND 2、肌细胞特异性增强因子2C（MEF 2C）和T-box 5（TBX 5））和microRNA（miR-1、miR-133、miR-208和miR-499）而恢复。通过激活参与胚胎心脏生长的有丝分裂信号通路刺激心肌细胞去分化和增殖代表了心脏再生和修复的补充方法。最近在了解心脏发育的机制基础方面的进展为心力衰竭的有效治疗提供了令人兴奋的机会。
As the adult mammalian heart has limited potential for regeneration and repair, the loss of cardiomyocytes during injury and disease can result in heart failure and death. The cellular processes and regulatory mechanisms involved in heart growth and development can be exploited to repair the injured adult heart through ‘reawakening’ pathways that are active during embryogenesis. Heart function has been restored in rodents by reprogramming non-myocytes into cardiomyocytes, by expressing transcription factors (GATA4, HAND2, myocyte-specific enhancer factor 2C (MEF2C) and T-box 5 (TBX5)) and microRNAs (miR-1, miR-133, miR-208 and miR-499) that control cardiomyocyte identity. Stimulating cardiomyocyte dedifferentiation and proliferation by activating mitotic signalling pathways involved in embryonic heart growth represents a complementary approach for heart regeneration and repair. Recent advances in understanding the mechanistic basis of heart development offer exciting opportunities for effective therapies for heart failure.
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影响因子：
64.5
作者：
Ginsberg M;James D;Ding BS;Nolan D;Geng F;Butler JM;Schachterle W;Pulijaal VR;Mathew S;Chasen ST;Xiang J;Rosenwaks Z;Shido K;Elemento O;Rabbany SY;Rafii S
通讯作者：
Rafii S
影响因子：
64.5
作者：
Bersell, Kevin;Arab, Shima;Kuehn, Bernhard
通讯作者：
Kuehn, Bernhard
影响因子：
2.7
作者：
GARCIAMARTINEZ, V;SCHOENWOLF, GC
通讯作者：
SCHOENWOLF, GC
影响因子：
5.3
作者：
EVANS, SM;TAI, LJ;CHIEN, KR
通讯作者：
CHIEN, KR
影响因子：
64.8
作者：
通讯作者：
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