ArticleNature cardiovascular research2024
YAP induces a neonatal-like pro-renewal niche in the adult heart.
Article in Nature cardiovascular research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 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.
The trial behind it
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
41 citing papers in PubMed, 47 citations in OpenAlex.
- Biomaterial-Assisted Stem Cell Therapy and Exosome Delivery in Myocardial Infarction: A Narrative Review.Biomimetics (Basel, Switzerland) · 2026Review
- Cardiac immunity and heart repair: Mechanism, challenge, and future direction.Chinese medical journal · 2026Review
- The emerging role of the Hippo signaling pathway in interorgan crosstalk.The FEBS journal · 2026Review
- YAP Induces a Prorenewal Metabolic State in Cardiomyocytes.Circulation · 2026Article
- Article
- TEAD-independent mechanisms of YAP function in cardiomyocyte cell cycle reentry.Life science alliance · 2026Article
- Epicardial Complement C3 Activation in Neonatal Cardiac Regeneration.Circulation · 2026Article
- Past, Present and Future of Regenerative Gene Therapy for Ischemic Heart Failure.Journal of cardiovascular translational research · 2026Review
- Ventricular assist device unloading reverses microvascular senescence in single ventricle disease.Nature cardiovascular research · 2026Article
- Single cell transcriptomic landscape of adult and pediatric non-ischemic cardiomyopathy.Journal of molecular and cellular cardiology · 2026Review
- Activation of developmental transcription factors using RNA technology promotes heart repair.bioRxiv : the preprint server for biology · 2026Article
- The Role of the C3a-C3aR Pathway in Diseases: Latest Research Advances.Mediators of inflammation · 2026Review
- YAP-Induced Glycolysis Drives Fibroinflammation and Disrupts Fibroblast Fidelity.Circulation research · 2025Article
- Reversible gene therapy for cardiac repair and protection.Nature cardiovascular research · 2025Article
- The multifaceted role of lactate in cardiovascular health: from metabolism to signaling and epigenetics.Epigenetics · 2025Review
- Gene therapy CM-YAPNature cardiovascular research · 2025Article
- Cardiomyocyte maturation and proliferation is a flip coin.BMC cardiovascular disorders · 2025Review
- YAP1 reactivation in cardiomyocytes following ECM remodelling contributes to the development of contractile force and sarcomere maturation.Cell death discovery · 2025Article
- Molecular gatekeepers of endogenous adult mammalian cardiomyocyte proliferation.Nature reviews. Cardiology · 2025Review
- Targeting the Hippo Pathway for Cardiac Regeneration.Physiology (Bethesda, Md.) · 2025Review
Corrections and comments
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Authors and funding
14 authors at 2 institutions in 2 countries.
Funding
Abstract
After myocardial infarction (MI), mammalian hearts do not regenerate, and the microenvironment is disrupted. Hippo signaling loss of function with activation of transcriptional co-factor YAP induces heart renewal and rebuilds the post-MI microenvironment. In this study, we investigated adult renewal-competent mouse hearts expressing an active version of YAP, called YAP5SA, in cardiomyocytes (CMs). Spatial transcriptomics and single-cell RNA sequencing revealed a conserved, renewal-competent CM cell state called adult (a)CM2 with high YAP activity. aCM2 co-localized with cardiac fibroblasts (CFs) expressing complement pathway component C3 and macrophages (MPs) expressing C3ar1 receptor to form a cellular triad in YAP5SA hearts and renewal-competent neonatal hearts. Although aCM2 was detected in adult mouse and human hearts, the cellular triad failed to co-localize in these non-renewing hearts. C3 and C3ar1 loss-of-function experiments indicated that C3a signaling between MPs and CFs was required to assemble the pro-renewal aCM2, C3+ CF and C3ar1+ MP cellular triad.
Identifiers
What OpenQuestion holds
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.