由線粒體呼吸產(chǎn)生的能量對于心臟功能而言是必需的，在2008年10月14日出版的《發(fā)育細胞》（Developmental Cell）上,，來自澳大利亞和美國的一組科學(xué)家發(fā)現(xiàn)哺乳動物胚胎心臟在受損傷之后會增加心肌細胞生成。
在研究過程中,，研究人員利用了一種心臟特異性技術(shù)來敲除負責(zé)編譯全細胞色素C合成酶（holocytochrome c synthase Hccs）的X連鎖基因,，全細胞色素C合成酶是一種激活呼吸細胞色素C和C1的酶。結(jié)果科學(xué)家們發(fā)現(xiàn),，由于該基因是X染色體連鎖的，因此進行基因敲除之后,，雌性小鼠能存活下來,，這是由于雌性擁有兩個X染色體，因此受損的基因表達能得到另一個X基因的補償,。與此相反,，雄性小鼠由于僅有的一個X連鎖基因受到破壞，因此心肌細胞功能變得不正常,，所以雄性小鼠會死亡,。
對于胚胎的分析證實了Hccs缺陷細胞和正常心肌細胞之間的50:50的比例，這和科學(xué)家們預(yù)期是一致的,?？茖W(xué)家們發(fā)現(xiàn)出生時受損的心臟組織僅僅占到心臟組織的10%，并且剩余的正常心肌組織能通過不斷的分裂增生,，最終形成一個功能正常的心臟,。然而盡管如此，長大的小鼠最終大部分仍然死于相關(guān)心臟疾病,，正常心肌組織的再生并不能完全消除受損心肌細胞帶來的傷害,。
文章作者最后認為,，以上發(fā)現(xiàn)表明胎兒的心臟具有令人驚訝的再生能力，能對心臟多達一半組織的損傷進行修復(fù),，這為治療人類的多種心臟疾病帶來了幫助,。（生物谷Bioon.com）
生物谷推薦原始出處：
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.
