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Evaluation of the molecular mechanisms by which serelaxin mediates its anti-fibrotic actions

thesis
posted on 23.07.2020 by CHAO WANG
Fibrosis (tissue scarring) is a hallmark of several cardiovascular diseases and cause of heart failure. Despite the significant burden of fibrosis, there are currently no effective cures for its regression. This thesis investigated novel signal transduction mechanisms by which the emerging anti-fibrotic drug, serelaxin, reduced fibrosis and related cardiac remodelling/function in primary human cardiac myofibroblasts (key fibrosis-producing cells) and a pre-clinical model of cardiomyopathy; and demonstrated the extent to which these cardioprotective effects of serelaxin could be enhanced by co-administration of the clinically-used anti-oxidant, N-Acetyl cysteine. These studies have contributed to developing serelaxin as a treatment for human heart diseases.

History

Principal supervisor

Chrishan Samuel

Additional supervisor 1

Barbara Kemp-Harper

Year of Award

2020

Department, School or Centre

Pharmacology

Campus location

Australia

Course

Doctor of Philosophy

Degree Type

DOCTORATE

Exports