西亚试剂：Compensatory Growth of Healthy Cardiac Cells in the Presenc

发布时间：2025-09-20

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.

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