ArticleMolecular therapy : the journal of the American Society of Gene Therapy2019
Long Non-coding RNA ECRAR Triggers Post-natal Myocardial Regeneration by Activating ERK1/2 Signaling.
Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 1 of them a synthesis that pooled it.
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Who cites it
59 citing papers in PubMed, 1 synthesis or guideline pooled it, 91 citations in OpenAlex.
- The Role of Long Noncoding RNAs in Cardiomyocyte Proliferation and Heart Regeneration After Myocardial Infarction: A Systematic Review.Cell transplantationPooled it
- Signaling pathways regulating cardiac regeneration.Cell regeneration (London, England) · 2026Review
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- Long non-coding RNAs as modulators of metabolic reprogramming for endogenous heart regeneration: Mechanisms and therapeutic potential.Biomedical journal · 2026Review
- CELF1 Downregulation Promotes Cardiomyocyte Hypertrophy via Regulating Alternative Splicing of Tead1.Genes · 2026Article
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- LncRNA HSCHARME is altered in human cardiomyopathies and promotes stem cell-derived cardiomyogenesis via splicing regulation.Nature communications · 2025Article
- The role of long non-coding RNAs in cardiovascular diseases: A comprehensive review.Non-coding RNA research · 2025Review
- Regenerative therapies for myocardial infarction: exploring the critical role of energy metabolism in achieving cardiac repair.Frontiers in cardiovascular medicine · 2025Review
- Trametinib, an anti-tumor drug, promotes oligodendrocytes generation and myelin formation.Acta pharmacologica Sinica · 2024Article
- Exploring the therapeutic potential of simvastatin in pancreatic neuroendocrine neoplasms: insights into cell cycle regulation and apoptosis.Translational cancer research · 2024Article
- Tert promotes cardiac regenerative repair after MI through alleviating ROS-induced DNA damage response in cardiomyocyte.Cell death discovery · 2024Article
- 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
- Targeting cardiomyocyte cell cycle regulation in heart failure.Basic research in cardiology · 2024Review
- Long non-coding RNAs in cardiac hypertrophy and heart failure: functions, mechanisms and clinical prospects.Nature reviews. Cardiology · 2024Review
- CDC-like kinase 3 deficiency aggravates hypoxia-induced cardiomyocyte apoptosis through AKT signaling pathway.In vitro cellular & developmental biology. Animal · 2024Article
- Biosafe cerium oxide nanozymes protect human pluripotent stem cells and cardiomyocytes from oxidative stress.Journal of nanobiotechnology · 2024Article
- Cardiac regeneration: Pre-existing cardiomyocyte as the hub of novel signaling pathway.Genes & diseases · 2024Review
- lncRNAs regulate cell stemness in physiology and pathology during differentiation and development.American journal of stem cells · 2024Review
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Reactivating post-natal myocardial regeneration potential may be a feasible strategy to regenerate the injured adult heart. Long non-coding RNAs (lncRNAs) have been implicated in regulating cellular differentiation, but whether they can elicit a regenerative response in the post-natal heart remains unknown. In this study, by characterizing the lncRNA transcriptome in human hearts during the fetal-to-adult transition, we found that 3,092 lncRNAs were differentially expressed, and we further identified a novel upregulated fetal lncRNA that we called endogenous cardiac regeneration-associated regulator (ECRAR), which promoted DNA synthesis, mitosis, and cytokinesis in post-natal day 7 and adult rat cardiomyocytes (CMs). Overexpression of ECRAR markedly stimulated myocardial regeneration and induced recovery of cardiac function after myocardial infarction (MI). Knockdown of ECRAR inhibited post-natal day 1 CM proliferation and prevented post-MI recovery. ECRAR was transcriptionally upregulated by E2F transcription factor 1 (E2F1). In addition, ECRAR directly bound to and promoted the phosphorylation of extracellular signal-regulated kinases 1 and 2 (ERK1/2), resulting in downstream targets of cyclin D1 and cyclin E1 activation, which, in turn, activated E2F1. The E2F1-ECRAR-ERK1/2 signaling formed a positive feedback loop to drive cell cycle progression, and, therefore, it promoted CM proliferation. These findings indicated that our newly discovered ECRAR may be a valuable therapeutic target for heart failure.
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