Ubiquitin ligase gene deletion attenuates diastolic dysfunction in pressure-overload hypertrophy.

Heart failure with a preserved left ventricular (LV) ejection fraction (HFpEF) often arises from a prolonged LV pressure overload (LVPO) and accompanied by abnormal extracellular matrix (ECM) accumulation. The E ubiquitin ligase WWP1 is a fundamental determinant ECM turnover. We tested the hypothesis that genetic ablation of would alter the progression of LVPO-induced HFpEF.