JOIN USEver wondered why a newborn animal's heart can heal itself completely whereas the adult organ lacks this ability? Oxygen may be to blame!
Scientists at University of Texas Southwestern Medical Center have unveiled why the heart loses its incredible regenerative capability in adulthood.
It is well-known that a major function of the heart is to circulate oxygen-rich blood throughout the body.
But at the same time, oxygen is a highly reactive, nonmetallic element and oxidising agent that readily forms toxic substances with many other compounds.
This latter property has now been found to underlie the loss of regenerative capacity in the adult heart.
The new finding shows that the oxygen-rich postnatal environment results in cell cycle arrest of cardiomyocytes, or heart cells.
"Knowing the key mechanism that turns the heart's regenerative capacity off in newborns tells us how we might discover methods to reawaken that capacity in the adult mammalian heart," said Dr Hesham Sadek, senior author of the study.
Due to the oxygen-rich atmosphere experienced immediately after birth, heart cells build up mitochondria - the powerhouse of the cell - which results in increased oxidisation.
The mass production of oxygen radicals by mitochondria damages DNA and, ultimately, causes cell cycle arrest.
"We have uncovered a previously unrecognised protective mechanism that mediates cardiomyocyte cell cycle arrest and that arises as a consequence of oxygen-dependent aerobic metabolism," said Sadek.
Physiologically speaking, Sadek said, mammals likely had to make the choice early on between being energy efficient or retaining the heart's ability to regenerate.
"The choice was clear. More than any organ in the body, the heart needs to be energy efficient in order to pump blood throughout life," said Sadek.
Heart muscle contains the highest amount of mitochondria in the body and consumes 30 per cent of the body's total oxygen in a resting state alone.
Unfortunately, the energy that comes from massive oxygen consumption comes with a price in the form of oxidation of DNA that makes the heart cells unable to divide and regenerate.
The finding was published in the journal Cell.