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

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.