ArticleNature genetics2017
Frequency of mononuclear diploid cardiomyocytes underlies natural variation in heart regeneration.
Article in Nature genetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 224 papers.
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Who cites it
224 citing papers in PubMed.
- High levels of the cardiomyocyte-specific kinase Tnni3k impair zebrafish heart regeneration by driving chronic myocardial inflammation.bioRxiv : the preprint server for biology · 2026Article
- Article
- Derivation of human post-mitotic cardiomyocytes from tetraploid iPSCs.Communications biology · 2026Article
- Epigenetic Control of Mammalian Cardiomyocyte Proliferation.Current cardiology reports · 2026Review
- Genome-wide association mapping and targeted loss of function studies identifyProceedings of the National Academy of Sciences of the United States of America · 2026Article
- The PIDDosome controls cardiomyocyte polyploidization during postnatal heart development.Cell death and differentiation · 2026Article
- Genes for 5'mRNA cap binding proteins, eif4ea and eif4eb, have alternative roles during heart regeneration.Developmental biology · 2026Article
- Review
- Mechanisms and Therapeutic Potential of Human Cardiomyocyte Proliferation.Journal of cardiovascular development and disease · 2026Review
- Tnni3k Is Cardioprotective in Viral Myocarditis.Journal of cardiovascular development and disease · 2026Article
- Distinct p21 dynamics drive alternative routes to whole-genome duplication through a common CDK4/6-dependent polyploid G0 state.bioRxiv : the preprint server for biology · 2026Article
- Insights into Cardiomyocyte Regeneration from Screening and Transcriptomics Approaches.International journal of molecular sciences · 2026Review
- Accumulation of newly synthesized docosahexaenoic acid plays an essential role in heart regeneration.Protein & cell · 2026Article
- Placental insufficiency disrupts cardiomyocyte ploidy and cell cycle fate in growth-restricted fetal sheep.American journal of physiology. Regulatory, integrative and comparative physiology · 2026Article
- Transient overexpression of hPKM2 in porcine cardiomyocytes prevents heart failure after myocardial infarction.Nature communications · 2025Article
- Cardiomyocyte maturation and proliferation is a flip coin.BMC cardiovascular disorders · 2025Review
- Squamate ventricular cardiomyocytes: Ploidy, proliferation, and heart muscle cell size in the leopard gecko (Eublepharis macularius).Developmental dynamics : an official publication of the American Association of Anatomists · 2025Article
- Molecular gatekeepers of endogenous adult mammalian cardiomyocyte proliferation.Nature reviews. Cardiology · 2025Review
- Flow cytometry of the myocardium: An end-to-end analysis of adult cardiomyocytes isolated from pig and mouse hearts.Journal of molecular and cellular cardiology · 2025Article
- Targeting Cardiomyocyte PCNA and POLD1 Prevents Pathologic Myocardial Hypertrophy.Circulation research · 2025Article
164 more citing papers are in PubMed but not listed here.
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19 authors.
Funding
Abstract
Adult mammalian cardiomyocyte regeneration after injury is thought to be minimal. Mononuclear diploid cardiomyocytes (MNDCMs), a relatively small subpopulation in the adult heart, may account for the observed degree of regeneration, but this has not been tested. We surveyed 120 inbred mouse strains and found that the frequency of adult mononuclear cardiomyocytes was surprisingly variable (>7-fold). Cardiomyocyte proliferation and heart functional recovery after coronary artery ligation both correlated with pre-injury MNDCM content. Using genome-wide association, we identified Tnni3k as one gene that influences variation in this composition and demonstrated that Tnni3k knockout resulted in elevated MNDCM content and increased cardiomyocyte proliferation after injury. Reciprocally, overexpression of Tnni3k in zebrafish promoted cardiomyocyte polyploidization and compromised heart regeneration. Our results corroborate the relevance of MNDCMs in heart regeneration. Moreover, they imply that intrinsic heart regeneration is not limited nor uniform in all individuals, but rather is a variable trait influenced by multiple genes.
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