由线粒体呼吸产生的能量对于心脏功能而言是必需的，在2008年10月14日出版的《发育细胞》（Developmental Cell）上，来自澳大利亚和美国的一组科学家发现哺乳动物胚胎心脏在受损伤之后会增加心肌细胞生成。
在研究过程中，研究人员利用了一种心脏特异性技术来敲除负责编译全细胞色素C合成酶（holocytochrome c synthase Hccs）的X连锁基因，全细胞色素C合成酶是一种激活呼吸细胞色素C和C1的酶。结果科学家们发现，由于该基因是X染色体连锁的，因此进行基因敲除之后，雌性小鼠能存活下来，这是由于雌性拥有两个X染色体，因此受损的基因表达能得到另一个X基因的补偿。与此相反，雄性小鼠由于仅有的一个X连锁基因受到破坏，因此心肌细胞功能变得不正常，所以雄性小鼠会死亡。
对于胚胎的分析证实了Hccs缺陷细胞和正常心肌细胞之间的50:50的比例，这和科学家们预期是一致的。科学家们发现出生时受损的心脏组织仅仅占到心脏组织的10%，并且剩余的正常心肌组织能通过不断的分裂增生，最终形成一个功能正常的心脏。然而尽管如此，长大的小鼠最终大部分仍然死于相关心脏疾病，正常心肌组织的再生并不能完全消除受损心肌细胞带来的伤害。
文章作者最后认为，以上发现表明胎儿的心脏具有令人惊讶的再生能力，能对心脏多达一半组织的损伤进行修复，这为治疗人类的多种心脏疾病带来了帮助。（生物谷Bioon.com）
生物谷推荐原始出处：
Developmental Cell，Vol 15, 521-533, 14 October 2008，J?rg-Detlef Drenckhahn, Timothy C. Cox
Compensatory Growth of Healthy Cardiac Cells in the Presence of Diseased Cells Restores Tissue Homeostasis during Heart Development
J?rg-Detlef Drenckhahn,1,2,3 Quenten P. Schwarz,2,9 Stephen Gray,1 Adrienne Laskowski,4 Helen Kiriazis,5 Ziqiu Ming,5 Richard P. Harvey,6 Xiao-Jun Du,5 David R. Thorburn,4,7 and Timothy C. Cox1,2,8,
1 Department of Anatomy & Developmental Biology, Monash University, Wellington Road, Clayton VIC 3800, Melbourne, Australia
2 School of Biomedical and Molecular Science, University of Adelaide, North Terrace, Adelaide SA 5005, Adelaide, Australia
3 Max-Delbrück Center for Molecular Medicine, Robert-R?ssle-Stra?e 10, 13125 Berlin, Germany
4 Murdoch Children's Research Institute, Royal Children's Hospital, Flemington Road, Parkville VIC 3052, Melbourne, Australia
5 Baker IDI Heart Research and Diabetes Institute, Commercial Road, Melbourne VIC 3004, Melbourne, Australia
6 Victor Chang Cardiac Research Institute, Liverpool Street, Darlinghurst NSW 2010, Sydney, Australia
7 Department of Paediatrics, University of Melbourne, Parkville VIC 3052, Melbourne, Australia
8 Division of Craniofacial Medicine, Department of Pediatrics, University of Washington, Seattle, WA 98195, USA
Summary
Energy generation by mitochondrial respiration is an absolute requirement for cardiac function. Here, we used a heart-specific conditional knockout approach to inactivate the X-linked gene encoding Holocytochrome c synthase (Hccs), an enzyme responsible for activation of respiratory cytochromes c and c1. Heterozygous knockout female mice were thus mosaic for Hccs function due to random X chromosome inactivation. In contrast to midgestational lethality of Hccs knockout males, heterozygous females appeared normal after birth. Analyses of heterozygous embryos revealed the expected 50:50 ratio of Hccs deficient to normal cardiac cells at midgestation; however, diseased tissue contributed progressively less over time and by birth represented only 10% of cardiac tissue volume. This change is accounted for by increased proliferation of remaining healthy cardiac cells resulting in a fully functional heart. These data reveal an impressive regenerative capacity of the fetal heart that can compensate for an effective loss of 50% of cardiac tissue.
