Heart to heart: grafting cardiosphere-derived cells augments cardiac self-repair by both myocytes and stem cells.
Heart to heart: grafting cardiosphere-derived cells augments cardiac self-repair by both myocytes and stem cells.
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DOI：
10.1002/emmm.201202345
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发表时间：
2013-02
影响因子：
11.1
通讯作者：
Schneider, Michael D.
中科院分区：
文献类型：
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作者：
Palacios, Jose A.;Schneider, Michael D.
与蝾螈和斑马鱼等高度再生的生物体相比（Kikuchi & Poss，2012），哺乳动物成年心脏组织的自我修复能力不足以重建心肌梗塞中损失的肌肉，阻碍心脏病发作和慢性心力衰竭中发生的细胞损失的功能恢复（Mercola等，2011）。成人心肌细胞中细胞周期退出的不可逆性在很大程度上阻碍了通过预先形成的心肌细胞的增殖来恢复泵功能。然而，推翻或灭活肿瘤抑制口袋蛋白是在成人心脏中设计持久循环的一种途径（Mercola等人，2011），并且小鼠中的命运图谱（Hsieh等人，2007）和人类心脏组织中的14C测年（Bergmann等人，2009）已证明持续的心肌细胞生成水平较低。虽然相当有限，但至少在健康衰老的心脏中，这种转变在概念上很重要，因为潜在的机制可能会被身体本身或临床医生在受伤后利用。这些心肌细胞从何而来，疾病中心肌细胞的生成程度如何？在成人心脏中发现具有心源性潜力的休眠或潜伏细胞表明了一个高度合理的来源（Mercola 等人，2011）。这些细胞通过多种方式纯化，共同表达许多心脏形成转录因子，并且已经报道了使用它们作为自体细胞产品的令人鼓舞的 I 期试验（SCIPIO，CADUCEUS；Bolli 等人，2011；Makkar 等人，2012）。或者，斑马鱼心脏的强健无疤愈合是通过分化的肌细胞重新进入细胞周期而发生的（Kikuchi & Poss，2012），这种机制仅适用于小鼠在生命的最初几天（Porrello 等，2011）。这些发现已经刺激了心肌细胞周期研究的复兴，寻求安全、可控的方法来重新启动成体心肌细胞的增殖（Eulalio 等，2012）。但是，是循环的可塑性还是分化的可塑性在受伤的心脏中产生了新的心肌细胞呢？
Compared with highly regenerative organisms such as newts and zebrafish (Kikuchi & Poss, 2012), the capacity of mammalian adult heart tissue to undergo self-repair is insufficient to reconstitute the muscle lost in myocardial infarction, hindering functional recovery from heart attacks and from cell loss occurring in chronic heart failure (Mercola et al, 2011). The irreversibility of cell cycle exit in adult cardiomyocytes largely prevents the restoration of pump function via proliferation of pre-formed myocytes. However, overriding or inactivating tumour suppressor pocket proteins is one route to engineer persistent cycling in the adult heart (Mercola et al, 2011), and low levels of on-going myocyte generation have been demonstrated by fate-mapping in mice (Hsieh et al, 2007) and 14C dating in human heart tissue (Bergmann et al, 2009). Although quite limited, at least in healthy aging hearts, such turnover is conceptually important, as the underlying mechanism (s) could potentially be exploited by the body itself or the clinician after injury. Where do such myocytes come from, and what is the extent of cardiomyocyte generation in disease? A highly plausible source is suggested by the discovery of dormant or latent cells with cardiogenic potential in adult hearts (Mercola et al, 2011). Purified by a variety of means, these cells have in common the expression of many heart-forming transcription factors, and encouraging phase I trials have been reported using them as autologous cell products (SCIPIO, CADUCEUS; Bolli et al, 2011; Makkar et al, 2012). Alternatively, the robust scarless healing of the heart in zebrafish occurs by differentiated myocytes re-entering the cell cycle (Kikuchi & Poss, 2012), a mechanism that is available to mice only during the first days of life (Porrello et al, 2011). These findings have already spurred a renaissance of cardiac cell cycle studies, seeking safe, controllable means to restart proliferation in adult cardiomyocytes (Eulalio et al, 2012). But is it the plasticity of cycling or the plasticity of differentiation that gives rise to new cardiomyocytes in injured hearts?
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影响因子：
168.9
作者：
Makkar, Raj R.;Smith, Rachel R.;Cheng, Ke;Malliaras, Konstantinos;Thomson, Louise E. J.;Berman, Daniel;Czer, Lawrence S. C.;Marban, Linda;Mendizabal, Adam;Johnston, Peter V.;Russell, Stuart D.;Schuleri, Karl H.;Lardo, Albert C.;Gerstenblith, Gary;Marban, Eduardo
通讯作者：
Marban, Eduardo
影响因子：
64.8
作者：
通讯作者：
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DOI：
10.1146/annurev-cellbio-101011-155739
发表时间：
2012
影响因子：
11.3
作者：
Kikuchi K;Poss KD
通讯作者：
Poss KD
影响因子：
64.8
作者：
Eulalio, Ana;Mano, Miguel;Giacca, Mauro
通讯作者：
Giacca, Mauro
影响因子：
16.6
作者：
通讯作者：
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