Some organs in the human body, such as the liver, can regenerate themselves after an injury; however, the heart cannot. Damage from a heart attack is permanent; thus, the health of individuals is often compromised after a heart attack. On August 8, 2011, UCLA stem cell researchers published a study in the Journal of Cell Biology, which shed light on the reason why the adult human heart cannot regenerate itself. The study, conducted in human cell lines and mice, may lead to methods of reprogramming a patient’s own cardiac myocytes within the heart itself to create new muscle to repair damage, said Dr. Robb MacLellan, a researcher with the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA and senior author of the study. Unlike newts and salamanders, human adults cannot spontaneously regrow damaged organs such as the heart. However, recent research suggests that mammals do have the ability to regenerate the heart for a very brief period, about the first week of life. However, that ability is quickly lost. But if we had it once, Dr. MacLellan said, maybe it is possible to regain that ability.
During human development, cardiac myocytes are made by progenitor stem cells and proliferate to form the heart. Once the heart is formed, the myocytes transform from immature cells into mature cells that cannot proliferate. That is not so for newts and salamanders, whose cardiac myocytes can go back and forth between immature, or primitive, states to proliferate and repair damage and then revert back into mature cells once the damage is repaired. Dr. MacLellan believes the reason adult human cardiac myocytes cannot do this is quite simple: when the myocytes are in a more primitive state, they are not as good at contracting, which is vital for proper heart function. Because humans are much larger than newts and salamanders, they need more heart contraction to maintain optimum blood pressure and circulation.
Dr. MacLellan said that by temporarily knocking down the proteins that block the cell cycle mechanism, it may be possible to get adult cardiac myocytes to re-enter the cell cycle and revert to a state where they can again proliferate. These therapies would need to be reversible so that the effects of the protein manipulation eventually wear off once the damage is repaired. Then myocytes would become mature again and aid in contracting the regenerated heart muscle. MacLellan currently is looking into using nanoparticles to deliver small interfering RNA to the heart to knock out the proteins that are keeping the myocytes mature.
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