ArticleNature cardiovascular research2025
The highly conserved PIWI-interacting RNA CRAPIR antagonizes PA2G4-mediated NF110-NF45 disassembly to promote heart regeneration in mice.
Article in Nature cardiovascular research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed.
- Molecular gatekeepers of endogenous adult mammalian cardiomyocyte proliferation.Nature reviews. Cardiology · 2025Review
- AGAPIR: A Novel PIWI-Interacting RNA Enhancing Post-Decompression Angiogenesis in Degenerative Cervical Myelopathy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The PIWI-interacting RNA CRAPIR alleviates myocardial ischemia‒reperfusion injury by reducing p53-mediated apoptosis via binding to SRSF1.Acta pharmacologica Sinica · 2025Article
- Cardiomyocyte regeneration: lessons from neonatal hearts.Regenerative medicine · 2025Article
- Powering up piRNAs for heart regeneration.Nature cardiovascular research · 2025Article
- Stem-Cell Derived Exosomal microRNAs as Biomarkers and Therapeutics for Pediatric Cardiovascular Disease.Current treatment options in cardiovascular medicine · 2025Review
Corrections and comments
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Authors and funding
19 authors.
Funding
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Abstract
Targeting the cardiomyocyte cell cycle is a promising strategy for heart repair following injury. Here, we identify a cardiac-regeneration-associated PIWI-interacting RNA (CRAPIR) as a regulator of cardiomyocyte proliferation. Genetic ablation or antagomir-mediated knockdown of CRAPIR in mice impairs cardiomyocyte proliferation and reduces heart regenerative potential. Conversely, overexpression of CRAPIR promotes cardiomyocyte proliferation, reduces infarct size and improves heart function after myocardial infarction. Mechanistically, CRAPIR promotes cardiomyocyte proliferation by competing with NF110 for binding to the RNA-binding protein PA2G4, thereby preventing the interaction of PA2G4 with the NF110-NF45 heterodimer and reducing NF110 degradation. The ability of CRAPIR to promote proliferation was confirmed in human embryonic stem cell-derived cardiomyocytes. Notably, CRAPIR serum levels are lower in individuals with ischemic heart disease and negatively correlate with levels of N-terminal pro-brain natriuretic peptide. These findings position CRAPIR both as a potential diagnostic marker for cardiac injury and as a therapeutic target for heart regeneration through the PA2G4-NF110-NF45 signaling axis.
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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.