ArticleAmerican journal of physiology. Heart and circulatory physiology2020
The ubiquitin ligase WWP1 contributes to shifts in matrix proteolytic profiles and a myocardial aging phenotype with diastolic heart.
Article in American journal of physiology. Heart and circulatory physiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Identification and validation of an interaction between the E3 ubiquitin ligase WWP1 and the Transcriptional Co-Activator WBP2 in the human heart.Biology open · 2026Article
- Modifying the structural substrate and progression of heart failure with preserved ejection fraction using a regular exercise regimen in pigs.American journal of physiology. Heart and circulatory physiology · 2026Article
- Identification and validation of the cellular senescence-associated molecular pattern and diagnostic markers for osteoporosis.BMC medical genomics · 2025Article
- Ubiquitination-mediated protein homeostasis in cardiovascular diseases: molecular mechanisms and therapeutic opportunities.American journal of cardiovascular disease · 2025Review
- Novel Therapeutic Avenues for Hypertrophic Cardiomyopathy.American journal of cardiovascular drugs : drugs, devices, and other interventions · 2023Review
- Ubiquitin ligaseAmerican journal of physiology. Heart and circulatory physiology · 2021Article
- The Role of HECT-Type E3 Ligase in the Development of Cardiac Disease.International journal of molecular sciences · 2021Review
- From Systemic Inflammation to Myocardial Fibrosis: The Heart Failure With Preserved Ejection Fraction Paradigm Revisited.Circulation research · 2021Review
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Ubiquitylation is a key event that regulates protein turnover, and induction of the ubiquitin ligase E3 WWP1 has been associated with age. Left ventricular hypertrophy (LVH) commonly occurs as a function of age and can cause heart failure (HF) with a preserved ejection fraction (EF; HFpEF). We hypothesized that overexpression (O/E) of WWP1 in the heart would cause LVH as well as functional and structural changes consistent with the aging HFpEF phenotype. Global WWP1 O/E was achieved in mice (
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Registered trials
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