Washington, April 25 (IANS): Know why newborn animal's heart can heal itself completely but the adult heart lacks this ability? The answer is in oxygen.
A ground-breaking research at University of Texas has revealed why the heart loses its incredible regenerative capability in adulthood.
“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,” explained Hesham Sadek, an assistant professor of internal medicine at UT Southwestern Medical Center.
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, non-metallic 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.
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, the study said.
“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,” Sadek noted.
In lab experiments, Sadek and his team found that if they subjected mice to a low-oxygen atmosphere, the cardiomyocytes divided longer than normal.
The opposite was true when mice were born in a higher-oxygenated atmosphere.
In that case, the cardiomyocytes stopped dividing earlier than normal.
Because the adult heart is not able to regenerate following injury, this represents a major barrier in cardiovascular medicine.
“Having a promising new understanding of what arrests cardiomyocyte cell cycle could be an important component of cardiomyocyte proliferation-based therapeutic approaches,” Sadek emphasised.
The research has been published in the journal Cell.