In:
eLife, eLife Sciences Publications, Ltd, Vol. 4 ( 2015-08-06)
Abstract:
Muscle cells in the heart contract in regular rhythms to pump blood around the body. In humans, rats and other mammals, the vast majority of heart muscle cells lose the ability to divide shortly after birth. Therefore, the heart is unable to replace cells that are lost over the life of the individual, for example, during a heart attack. If too many of these cells are lost, the heart will be unable to pump effectively, which can lead to heart failure. Currently, the only treatment option in humans with heart failure is to perform a heart transplant. Some animals, such as newts and zebrafish, are able to replace lost heart muscle cells throughout their lifetimes. Thus, these species are able to fully regenerate their hearts even after 20% has been removed. This suggests that it might be possible to manipulate human heart muscle cells to make them divide and regenerate the heart. Recent research has suggested that structures called centrosomes, known to be required to separate copies of the DNA during cell division, are used as a hub to integrate the initial signals that determine whether a cell should divide or not. Here, Zebrowski et al. studied the centrosomes of heart muscle cells in rats, newts and zebrafish. The experiments show that the centrosomes in rat heart muscle cells are dissembled shortly after birth. Centrosomes are made of several proteins and, in the rat cells, these proteins moved to the membrane that surrounded the nucleus. On the other hand, the centrosomes in the heart muscle cells of the adult newts and zebrafish remained intact. Further experiments found that that breaking apart the centrosomes of heart muscle cells taken from newborn rats stops these cells from dividing. Zebrowski et al.'s findings suggest that the loss of centrosomes after birth is a possible reason why the hearts of adult humans and other mammals are unable to regenerate after injury. In the future, these findings may aid the development of methods to regenerate human heart muscle and new treatments that may limit division of cancer cells.
Type of Medium:
Online Resource
ISSN:
2050-084X
DOI:
10.7554/eLife.05563.001
DOI:
10.7554/eLife.05563.002
DOI:
10.7554/eLife.05563.003
DOI:
10.7554/eLife.05563.004
DOI:
10.7554/eLife.05563.005
DOI:
10.7554/eLife.05563.006
DOI:
10.7554/eLife.05563.007
DOI:
10.7554/eLife.05563.008
DOI:
10.7554/eLife.05563.009
DOI:
10.7554/eLife.05563.010
DOI:
10.7554/eLife.05563.011
DOI:
10.7554/eLife.05563.012
DOI:
10.7554/eLife.05563.013
DOI:
10.7554/eLife.05563.014
DOI:
10.7554/eLife.05563.015
Language:
English
Publisher:
eLife Sciences Publications, Ltd
Publication Date:
2015
detail.hit.zdb_id:
2687154-3
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