Heart failure with a preserved left ventricular ejection fraction (HFpEF) often arises from a prolonged left ventricular pressure overload and is accompanied by abnormal extracellular matrix accumulation. In their recent study titled "Ubiquitin ligase Wwp1 gene deletion attenuates diastolic dysfunction in pressure-overload hypertrophy", Dr. Lydia Matesic and her colleagues at UofSC show that the genetic ablation of the E3 ubiquitin ligase WWP1 reduces the development of left ventricular hypertrophy and subsequent progression to HFpEF. Modulating the WWP1 pathway could thus be a therapeutic target to alter the natural history of HFpEF. A great work!
Department of Biological Sciences
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- Dr. Lydia Matesic and her colleagues published a new study in the American Journal of Physiology-Heart and Circulatory Physiology