Mammalian heart renewal by pre-existing cardiomyocytes.
Mammalian heart renewal by pre-existing cardiomyocytes.
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虽然最近的研究表明，心脏细胞在成年哺乳动物中产生，但新心脏细胞的产生频率和来源尚不清楚。一些研究表明，干细胞活性高，祖细胞分化为心肌细胞。其他研究表明，新的心肌细胞以非常低的速度出生，它们可能来自于预先存在的心肌细胞的分裂。在这里，我们表明，通过结合两种不同的脉冲追踪方法-遗传命运-映射与稳定同位素标记，和多同位素成像质谱-心肌细胞的发生率低，在正常衰老过程中，预先存在的心肌细胞的分裂，增加邻近心肌损伤区域的过程。我们发现，在正常衰老和损伤后的细胞周期活动导致多倍体和多核，但也导致新的二倍体，单核心肌细胞。这些数据揭示了预先存在的心肌细胞作为正常哺乳动物心肌稳态以及心肌损伤后心肌细胞替代的主要来源。
Although recent studies have revealed that heart cells are generated in adult mammals, the frequency of generation and the source of new heart cells are not yet known. Some studies suggest a high rate of stem cell activity with differentiation of progenitors to cardiomyocytes. Other studies suggest that new cardiomyocytes are born at a very low rate,,, and that they may be derived from the division of pre-existing cardiomyocytes. Here we show, by combining two different pulse–chase approaches—genetic fate-mapping with stable isotope labelling, and multi-isotope imaging mass spectrometry—that the genesis of cardiomyocytes occurs at a low rate by the division of pre-existing cardiomyocytes during normal ageing, a process that increases adjacent to areas of myocardial injury. We found that cell cycle activity during normal ageing and after injury led to polyploidy and multinucleation, but also to new diploid, mononucleate cardiomyocytes. These data reveal pre-existing cardiomyocytes as the dominant source of cardiomyocyte replacement in normal mammalian myocardial homeostasis as well as after myocardial injury.
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影响因子：
64.8
作者：
Zhang, Duan-Sun;Piazza, Valeria;Perrin, Benjamin J.;Rzadzinska, Agnieszka K.;Poczatek, J. Collin;Wang, Mei;Prosser, Haydn M.;Ervasti, James M.;Corey, David P.;Lechene, Claude P.
通讯作者：
Lechene, Claude P.
影响因子：
64.5
作者：
Wilson, Anne;Laurenti, Elisa;Trumpp, Andreas
通讯作者：
Trumpp, Andreas
DOI：
10.1073/pnas.0903089106
发表时间：
2009-10-06
影响因子：
11.1
作者：
Hosoda, Toru;D'Amario, Domenico;Leri, Annarosa
通讯作者：
Leri, Annarosa
影响因子：
37.8
作者：
Dong, Feng;Harvey, James;Penn, Marc S.
通讯作者：
Penn, Marc S.
影响因子：
64.8
作者：
通讯作者：
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