A study into the mitochondrial respiratory chain has shown that heart cells have an impressive regenerative capacity in embryonic mice.

Researchers from Monash University, the University of Adelaide, and the Baker Heart Institute and Murdoch Children’s Research Institute in Melbourne used a heart-specific knockout mouse model to study energy generation by mitochondrial respiration, which is essential to cardiac function.

The researchers generated mice with the gene encoding the Holocytochrome c synthase (Hccs) enzyme knocked out. The enzyme activates key respiratory proteins crucial for mitochondrial function.

The gene sits on the X chromosome, so hemizygous male embryos and homozygous female embryos died. Heterozygous female embryos, however, survived. At mid-gestation, the expected 50:50 ratio of Hccc deficient cells to normal cardiac cells was observed.

By birth, diseased tissue represented only 10 per cent of volume at birth.

The researchers say the data reveal an impressive regenerative capacity in the foetal heart in the face of extensive somatic disease.

“Compensatory growth of healthy cardiac cells in the presence of diseased cells restores tissue homeostasis during heart development”, by Jorg-Detlef Drenckhahn et al, is published in Developmental Cell [doi 10.1016/j.devcel.2008.09.005.]