Ubiquitin ligase Wwp1 gene deletion attenuates diastolic dysfunction in pressure-overload hypertrophy
Copyright policy )Ubiquitin ligase Wwp1 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 is accompanied by abnormal extracellular matrix (ECM) accumulation. It is now recognized that the ECM is a dynamic entity that is regulated at multiple post-transcriptional levels, including the E3 ubiquitin ligases, such as WWP1. In the present study, WWP1 deletion in the context of an LVPO stimulus reduced functional indices of HFpEF progression and determinants of ECM remodeling. Understanding and targeting the ubiquitin ligases in the context of HFpEF forms an important research direction.
- University of South Carolina System United States
- University of South Carolina United States
Heart Failure, Male, Mice, Knockout, Time Factors, Ventricular Remodeling, Fibrillar Collagens, Heart Ventricles, Ubiquitin-Protein Ligases, Ventricular Function, Left, Extracellular Matrix, Mice, Inbred C57BL, Disease Models, Animal, Ventricular Dysfunction, Left, Diastole, Disease Progression, Animals, Female, Hypertrophy, Left Ventricular, Aorta, Gene Deletion
Heart Failure, Male, Mice, Knockout, Time Factors, Ventricular Remodeling, Fibrillar Collagens, Heart Ventricles, Ubiquitin-Protein Ligases, Ventricular Function, Left, Extracellular Matrix, Mice, Inbred C57BL, Disease Models, Animal, Ventricular Dysfunction, Left, Diastole, Disease Progression, Animals, Female, Hypertrophy, Left Ventricular, Aorta, Gene Deletion
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