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dc.rights.licenseCC-BY-NC-ND
dc.contributor.advisorDansen, T.B.
dc.contributor.authorSoyal, M.
dc.date.accessioned2012-09-02T17:00:40Z
dc.date.available2012-09-02
dc.date.available2012-09-02T17:00:40Z
dc.date.issued2012
dc.identifier.urihttps://studenttheses.uu.nl/handle/20.500.12932/17800
dc.description.abstractAcute myocardial infarction (AMI) is a major cause of morbidity. AMI is caused by a blockage of one or multiple coronary arteries, leading to an ischemic (loss of blood flow) area of the heart. Restoring blood flow (reperfusion) to the ischemic area is the primary course of action when an AMI patient presents himself. Reperfusion of the infarcted area however causes injury to the previously ischemic area, meaning that the treatment itself is damaging to the myocardium. This damaging period is termed ischemia/reperfusion injury and the proposed processes propagating I/R injury will be described in this paper. Forkhead Box O (FOXO) family of transcription factors are regulators of many genes involved in processes like reactive oxygen species (ROS) scavenging, apoptosis, development and immunity. Almost all of the functions which can be exerted by FOXOs via their target genes can be related to I/R injury, as will be discussed in this paper. The primary goal of this paper is to give the reader better insight into the processes underlying I/R injury, and the functions and regulation of FOXOs. Can and should FOXOs, considering their numerous target genes, be targeted therapeutically to attenuate ischemia/reperfusion injury?
dc.description.sponsorshipUtrecht University
dc.format.extent546440 bytes
dc.format.mimetypeapplication/pdf
dc.language.isoen
dc.titleForkhead Box O in ischemia/reperfusion injury: a potential therapeutic target
dc.type.contentMaster Thesis
dc.rights.accessrightsOpen Access
dc.subject.keywordsAMI, FOXO, ischemia/reperfusion
dc.subject.courseuuBiology of Disease


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