Why the study?
HFpEF commonly afflicts the elderly and involves diastolic dysfunction and an abnormal ECM, while ubiquitin ligases such as WWP1 change with aging and regulate ECM turnover.
Does induction of WWP1 induce LV hypertrophy, diastolic dysfunction, and ECM accumulation in mice?
Does induction of WWP1 induce LV hypertrophy, diastolic dysfunction, and ECM accumulation in mice?
Induction of the ubiquitin ligase WWP1 in mice produces a phenotype consistent with HFpEF, identifying a potential new therapeutic pathway.
Heart failure (HF) with a preserved ejection fraction (HFpEF) is a growing cause of HF and commonly afflicts the elderly. Milestones for HFpEF include diastolic dysfunction and an abnormal extracellular matrix (ECM). The ubiquitin ligases, such as WWP1, change with aging and regulate critical protein turnover/stability processes, such as the ECM. The present study demonstrated that induction of WWP1 in mice induced LV hypertrophy, diastolic dysfunction, and ECM accumulation, consistent with the HFpEF phenotype, and thus may identify a new therapeutic pathway.
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Matesic et al. (2020) studied this question.
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