Researchers has revealed that the oxygen helps the heart lose its incredible regenerative capability in adulthood.
This groundbreaking new finding finds that the oxygen-rich postnatal environment results in cell cycle arrest of cardiomyocytes, or heart cells.
Dr. Hesham Sadek, Assistant Professor of Internal Medicine at UT Southwestern and senior author of the study, said knowing the key mechanism that turns the heart's regenerative capacity off in newborns tells them how they might discover methods to reawaken that capacity in the adult mammalian 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 oxidization. The mass production of oxygen radicals by mitochondria damages DNA and, ultimately, causes cell cycle arrest.
Dr Sadek said that they have uncovered a previously unrecognized protective mechanism that mediates cardiomyocyte cell cycle arrest and that arises as a consequence of oxygen-dependent aerobic metabolism.
Heart muscle contains the highest amount of mitochondria in the body and consumes 30 percent 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.
Dr. Sadek, along with co-first authors Dr. Bao "Robyn" Puente, postdoctoral trainee in Pediatrics, and Dr. Wataru Kimura, visiting senior researcher in Internal Medicine, found that if they subjected mice to a low-oxygen atmosphere, the cardiomyocytes divided longer than normal.
The study has been published in the journal Cell.
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