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dc.contributor.authorAbu Bakar, Nur Dianah Binte
dc.contributor.supervisorNina Tirnitz-Parkeren_US
dc.contributor.supervisorRodrigo Carlessien_US
dc.contributor.supervisorRicky Lareuen_US
dc.date.accessioned2025-07-30T01:23:36Z
dc.date.available2025-07-30T01:23:36Z
dc.date.issued2025en_US
dc.identifier.urihttp://hdl.handle.net/20.500.11937/98186
dc.description.abstract

Aspirin shows promise as an accessible approach for preventing liver disease and hepatocellular carcinoma (HCC). Using mouse models combining gene editing and a NASH-inducing diet, aspirin reduced liver inflammation, fibrosis, oxidative stress, and hypoxia, while shifting immune cell profiles toward tissue repair. Key targets included COX-1 and hypoxia pathways. These findings highlight aspirin’s potential as a protective agent in chronic liver disease management and warrant further investigation into its mechanisms and role in HCC prevention.

en_US
dc.publisherCurtin Universityen_US
dc.titleAspirin in a novel mouse model of metabolic steatotic liver disease and its potential to prevent hepatocellular carcinomaen_US
dc.typeThesisen_US
dcterms.educationLevelPhDen_US
curtin.departmentCurtin Medical Schoolen_US
curtin.accessStatusFulltext not availableen_US
curtin.facultyHealth Sciencesen_US
curtin.contributor.orcidAbu Bakar, Nur Dianah Binte [0000-0002-9047-5653]en_US
dc.date.embargoEnd2027-07-29


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