A recent research showed that embryonic mouse heart has the capacity to regenerate, a phenomenon that was till now attributed to non-mammalian species. The study was conducted by Professor Timothy C. Cox and his colleagues from the University of Washington in Seattle.

The study showed that the embryonic heart can replace diseased tissue through compensatory proliferation of healthy cells. Disorders of the mitochondria, a cell structure required for energy production, are one of the leading causes of early onset of fatal cardiomyopathies. 

This study was conducted to find how mutations, which interfere with mitochondrial function, impact the heart during development.

During the study, a heart-specific knockout approach was used in mice to inactivate a gene crucial for normal mitochondrial function. Experimental methods used by the researchers established embryonic female mice with mosaic hearts, composed of mixed cell populations: half normal and half "diseased". But at birth, the diseased cells represented only about 10 per cent of the cardiac tissue. 

The researchers found that increased proliferation of healthy heart cells was responsible for this change, and led to a fully functional heart. 

Researchers believe that despite normal cardiac function early in life, over 40 per cent of adult mice prematurely developed cardiac pathologies, which might indicate a hitherto unsuspected embryological origin for early onset cardiac disease in humans. 

Professor Cox said that our findings reveal an impressive regenerative capacity of the foetal heart that can compensate for an effective loss of half of the cardiac tissue.