Getting to the heart of cardiac repair

A surprising discovery suggests cardiac self-repair may be possible...
27 February 2011


A surprising discovery suggests cardiac self-repair may be possible.  Prevailing wisdom suggests that mammalian hearts like our own lack the capacity to self-repair if they are injured.  This is in stark contrast to other Human Heartanimals, including fish, that can regenerate up to a quarter of their heart muscle if it is injured or removed.  But now scientists have discovered that the newborn mammalian heart also initially has the ability to do the same, but only for a short while.

Writing in Science, University of Texas Southwestern Medical Center scientist Enzo Porrello and his colleagues removed about 15% of the muscle from the apices of the left ventricles of 1 day old mice.  After forming a blood clot to seal the wound at the site of the injury, the mouse hearts re-grew completely within 21 days, without the development of scar tissue and with the formation of new muscle tissue and blood vessels; functional tests carried out at two months also confirmed that the recovered hearts were beating completely normally.

The recovery was achieved, the scientists found, through the proliferation of surviving muscle cells elsewhere in the heart; newly-produced heart cells migrated to the site of the injury where they then wired themselves into the regenerating tissue to replace the lost muscle.  However, when the same procedure was attempted on slightly older, 7 day-old mouse pups, there was no such regenerative effort, the injured hearts developed significant scar tissue and failed to repair themselves.  This intriguing result shows that the mammalian heart is capable of self-repair similar to the hearts of simpler species like zebrafish but, for some reason, this capacity is lost soon after birth.

Encouragingly, however, it also suggests that if scientists can uncover the reason underlying this switch from a pro- to a non-repair state, using a model system like this, then it might be possible to trigger the same restoratative pathway in adult human victims of cardiac diseases.


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