p53 mediates cell death in the heart
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Date
2019
Authors
Roveimiab, Zeinab
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Abstract
During cellular stress, cells try to survive and overcome the stress by an essential process called autophagy. This process involves degrading and recycling organelles and macromolecules. Different human diseases such as heart failure are on the rise due to changes in our diet and these diseases can be worsened by defects in the regulation of this very important process, autophagy.
Doxorubicin as an antitumor drug induces tumor suppressor protein p53 activation in the heart, which causes mitochondria defects, autophagy and cell death in cardiomyocytes. Also, in this thesis, I found that overexpression of p53 increases the level of the autophagy marker, Beclin 1, that is activated in the autophagy’s first stage, which is the autophagosome formation, by making a double membrane structure that engulfs cytoplasmic material.
These data provide evidence that Doxorubicin induces p53 which activates autophagy and cardiomyocytes cell death. Therefore, the results of this thesis demonstrate that when p53 is activated, it can promote cardiomyocyte cell death through an autophagy dependent process during cardiac stress.
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Keywords
p53, Cell death, Heart, Autophagy
Citation
MLA