Foglia Matthew J, Poss Kenneth D
Department of Cell Biology, Duke University School of Medicine, Durham, NC 27710, USA.
Department of Cell Biology, Duke University School of Medicine, Durham, NC 27710, USA
Development. 2016 Mar 1;143(5):729-40. doi: 10.1242/dev.132910.
The adult human heart does not regenerate significant amounts of lost tissue after injury. Rather than making new, functional muscle, human hearts are prone to scarring and hypertrophy, which can often lead to fatal arrhythmias and heart failure. The most-cited basis of this ineffective cardiac regeneration in mammals is the low proliferative capacity of adult cardiomyocytes. However, mammalian cardiomyocytes can avidly proliferate during fetal and neonatal development, and both adult zebrafish and neonatal mice can regenerate cardiac muscle after injury, suggesting that latent regenerative potential exists. Dissecting the cellular and molecular mechanisms that promote cardiomyocyte proliferation throughout life, deciphering why proliferative capacity normally dissipates in adult mammals, and deriving means to boost this capacity are primary goals in cardiovascular research. Here, we review our current understanding of how cardiomyocyte proliferation is regulated during heart development and regeneration.
成年人类心脏在受伤后无法大量再生失去的组织。人类心脏不会生成新的功能性肌肉,而是容易形成瘢痕和肥大,这常常会导致致命的心律失常和心力衰竭。哺乳动物心脏再生无效最常被提及的原因是成年心肌细胞的增殖能力较低。然而,哺乳动物的心肌细胞在胎儿和新生儿发育期间能够快速增殖,成年斑马鱼和新生小鼠在受伤后都能再生心肌,这表明潜在的再生能力是存在的。剖析促进心肌细胞终生增殖的细胞和分子机制,解读成年哺乳动物增殖能力为何通常会消失,并找到增强这种能力的方法,是心血管研究的主要目标。在此,我们综述了目前对心脏发育和再生过程中心肌细胞增殖调控方式的理解。