ArticleNature communications2018
Loss of microRNA-128 promotes cardiomyocyte proliferation and heart regeneration.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 108 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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Who cites it
108 citing papers in PubMed, 160 citations in OpenAlex.
- A positively selected microRNA controls a reversible aging program in striated muscle.bioRxiv : the preprint server for biology · 2026Article
- Review
- Restoration of RBM22 overcomes the transcriptional and epigenetic barriers of cardiomyocyte proliferation for heart regeneration.Nature communications · 2026Article
- Activation of developmental transcription factors using RNA technology promotes heart repair.bioRxiv : the preprint server for biology · 2026Article
- Multi-Omics Evidence Based on Spatial Transcriptomics Data Reveals the Therapeutic Value of Copper Death Genes in Glioblastoma.International journal of genomics · 2026Article
- The Role of MicroRNAs in the Pathophysiology and Management of Heart Failure: From Molecular Mechanisms to Clinical Application.International journal of molecular sciences · 2025Review
- MicroRNAs in neurodegenerative diseases: from molecular mechanisms to clinical biomarkers, detection methods and therapeutic strategies-advances and challenges.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025Review
- Transcriptional, proteomic and metabolic drivers of cardiac regeneration.Heart (British Cardiac Society) · 2025Review
- Nuclear Autoantigenic Sperm Protein Promotes Cardiac Regeneration and Repair Through Activating the PDGFRB/AKT Pathway.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Cell Reprogramming, Transdifferentiation, and Dedifferentiation Approaches for Heart Repair.International journal of molecular sciences · 2025Review
- Regenerative therapies for myocardial infarction: exploring the critical role of energy metabolism in achieving cardiac repair.Frontiers in cardiovascular medicine · 2025Review
- Analysis of microRNA expression reveals convergent evolution of the molecular control of diapause in annual killifishes.Frontiers in genetics · 2025Article
- Cell cycle arrest of cardiomyocytes in the context of cardiac regeneration.Frontiers in cardiovascular medicine · 2025Review
- MicroRNA-specific therapeutic targets and biomarkers of apoptosis following myocardial ischemia-reperfusion injury.Molecular and cellular biochemistry · 2024Review
- Direct Cardiac Reprogramming in the Age of Computational Biology.Journal of cardiovascular development and disease · 2024Review
- Non-coding RNAs as therapeutic targets and biomarkers in ischaemic heart disease.Nature reviews. Cardiology · 2024Review
- Upregulation of LncRNA UCA1 promotes cardiomyocyte proliferation by inhibiting the miR-128/SUZ12/P27 pathway.Heliyon · 2024Article
- CircSorbs1 regulates myocardial regeneration and reduces cancer therapy-related cardiovascular toxicity through the Mir-99/GATA4 pathway.Discover oncology · 2024Article
- The role of miR-128 and MDFI in cardiac hypertrophy and heart failure: Mechanistic.Journal of cellular and molecular medicine · 2024Article
- Identification of circular RNAs regulating cardiomyocyte proliferation in neonatal pig hearts.JCI insight · 2024Article
48 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
18 authors at 7 institutions in 3 countries.
Funding
Abstract
The goal of replenishing the cardiomyocyte (CM) population using regenerative therapies following myocardial infarction (MI) is hampered by the limited regeneration capacity of adult CMs, partially due to their withdrawal from the cell cycle. Here, we show that microRNA-128 (miR-128) is upregulated in CMs during the postnatal switch from proliferation to terminal differentiation. In neonatal mice, cardiac-specific overexpression of miR-128 impairs CM proliferation and cardiac function, while miR-128 deletion extends proliferation of postnatal CMs by enhancing expression of the chromatin modifier SUZ12, which suppresses p27 (cyclin-dependent kinase inhibitor) expression and activates the positive cell cycle regulators Cyclin E and CDK2. Furthermore, deletion of miR-128 promotes cell cycle re-entry of adult CMs, thereby reducing the levels of fibrosis, and attenuating cardiac dysfunction in response to MI. These results suggest that miR-128 serves as a critical regulator of endogenous CM proliferation, and might be a novel therapeutic target for heart repair.
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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.