ArticleFrontiers in cardiovascular medicine2023
Myofibroblast Ccn3 is regulated by Yap and Wwtr1 and contributes to adverse cardiac outcomes.
Article in Frontiers in cardiovascular medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed, 7 citations in OpenAlex.
- The Role of the Cellular Communication Network Protein Family in Pulmonary Arterial Hypertension.Pulmonary circulation · 2026Article
- ANTXR1 blockade enhances cardiac function in preclinical models of heart failure.Nature cardiovascular research · 2025Article
- Targeting the Hippo Pathway for Cardiac Regeneration.Physiology (Bethesda, Md.) · 2025Review
- Cell type specificity of Hippo-YAP signaling in cardiac development and disease.Journal of molecular and cellular cardiology · 2025Review
- Cardiac Development, Cellular Composition and Function: From Regulatory Mechanisms to Applications.Cells · 2025Review
- The Multifaceted Roles of Hippo-YAP in Cardiovascular Diseases.Cardiovascular toxicology · 2024Review
- Integrative multi-omics profiling in human decedents receiving pig heart xenografts.Nature medicine · 2024Article
- Serum Levels of CCN3 Protein in Iranian Women with Polycystic Ovary Syndrome.Journal of reproduction & infertilityArticle
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 2 countries.
Funding
Abstract
Introduction: While Yap and Wwtr1 regulate resident cardiac fibroblast to myofibroblast differentiation following cardiac injury, their role specifically in activated myofibroblasts remains unexplored. Methods: We assessed the pathophysiological and cellular consequence of genetic depletion of Yap alone ( Results: Following myocardial infarction, depletion of Yap in myofibroblasts had minimal effect on heart function while depletion of Yap/Wwtr1 resulted in smaller scars, reduced interstitial fibrosis, and improved ejection fraction and fractional shortening. Single cell RNA sequencing of interstitial cardiac cells 7 days post infarction showed suppression of pro-fibrotic genes in fibroblasts derived from Discussion: Yap/Wwtr1 depletion in myofibroblasts attenuates fibrosis and significantly improves cardiac outcomes after myocardial infarction and we identify
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.