p53 mediates cell death in the heart

dc.contributor.authorRoveimiab, Zeinab
dc.contributor.examiningcommitteeDhingra, Sanjiv (Physiology and Pathophysiology) Wigle, Jeffrey (Biochemistry and Medical Genetics)en_US
dc.contributor.supervisorKirshenbaum, Lorrie ( Physiology and Pathophysiology)en_US
dc.date.accessioned2020-01-08T17:11:47Z
dc.date.available2020-01-08T17:11:47Z
dc.date.issued2019en_US
dc.date.submitted2019-11-21T02:31:27Zen
dc.degree.disciplinePhysiology and Pathophysiologyen_US
dc.degree.levelMaster of Science (M.Sc.)en_US
dc.description.abstractDuring 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.en_US
dc.description.noteFebruary 2020en_US
dc.identifier.citationMLAen_US
dc.identifier.urihttp://hdl.handle.net/1993/34460
dc.language.isoengen_US
dc.rightsopen accessen_US
dc.subjectp53en_US
dc.subjectCell deathen_US
dc.subjectHearten_US
dc.subjectAutophagyen_US
dc.titlep53 mediates cell death in the hearten_US
dc.typemaster thesisen_US
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