High circulating levels of fibroblast growth factor 23 (FGF23) have been linked to clinical cardiovascular events in patients with CKD. Experimental evidence indicates that FGF23 directly promotes left ventricle hypertrophy. Our lab has shown that both genetic deficiency and pharmacological inhibition of PAI-1 reduce FGF23 levels in different mouse models. In this project, we aim to use a transgenic mouse model that expresses a stable form of human PAI-1 to study the role of PAI-1 in CKD-associated cardiac hypertrophy and test the efficacy of an orally-active small molecule PAI-1 inhibitor in reducing FGF23-associated cardiac hypertrophy.
|Effective start/end date||1/1/19 → 12/31/20|
- American Heart Association (19PRE34381029)