ArticleCardiovascular research2018
Loss of AZIN2 splice variant facilitates endogenous cardiac regeneration.
Article in Cardiovascular research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 49 papers, 1 of them a synthesis that pooled it.
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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
49 citing papers in PubMed, 1 synthesis or guideline pooled it, 79 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
- Long non-coding RNAs as modulators of metabolic reprogramming for endogenous heart regeneration: Mechanisms and therapeutic potential.Biomedical journal · 2026Review
- Review
- LncRNA HSCHARME is altered in human cardiomyopathies and promotes stem cell-derived cardiomyogenesis via splicing regulation.Nature communications · 2025Article
- Regenerative therapies for myocardial infarction: exploring the critical role of energy metabolism in achieving cardiac repair.Frontiers in cardiovascular medicine · 2025Review
- Cell cycle arrest of cardiomyocytes in the context of cardiac regeneration.Frontiers in cardiovascular medicine · 2025Review
- Comprehensive Quality Analysis of Conventional and Novel Biomarkers in Diagnosing and Predicting Prognosis of Coronary Artery Disease, Acute Coronary Syndrome, and Heart Failure, a Comprehensive Literature Review.Journal of cardiovascular translational research · 2024Review
- Extracellular vesicle transfer of lncRNA H19 splice variants to cardiac cells.Molecular therapy. Nucleic acids · 2024Article
- Tert promotes cardiac regenerative repair after MI through alleviating ROS-induced DNA damage response in cardiomyocyte.Cell death discovery · 2024Article
- Non-Coding RNA-Mediated Gene Regulation in Cardiovascular Disorders: Current Insights and Future Directions.Journal of cardiovascular translational research · 2024Review
- Upregulation of LncRNA UCA1 promotes cardiomyocyte proliferation by inhibiting the miR-128/SUZ12/P27 pathway.Heliyon · 2024Article
- Long non-coding RNAs in cardiac hypertrophy and heart failure: functions, mechanisms and clinical prospects.Nature reviews. Cardiology · 2024Review
- Optogenetic Stimulation of the Cardiac Vagus Nerve to Promote Heart Regenerative Repair after Myocardial Infarction.International journal of biological sciences · 2024Article
- The role and medical prospects of long non-coding RNAs in cardiovascular disease.Heart failure reviews · 2023Review
- The Role of Long Non-Coding RNAs in Cardiovascular Diseases.International journal of molecular sciences · 2023Review
- New Insights into Pathophysiology and New Risk Factors for ACS.Journal of clinical medicine · 2023Review
- The Role of ncRNAs in Cardiac Infarction and Regeneration.Journal of cardiovascular development and disease · 2023Review
- Evaluating the Role of lncRNAs in the Incidence of Cardiovascular Diseases in Androgenetic Alopecia Patients.Cardiovascular toxicology · 2022Review
- Epigenetic regulation in cardiovascular disease: mechanisms and advances in clinical trials.Signal transduction and targeted therapy · 2022Review
Corrections and comments
- Commented on by
- Erratum issued
Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aims: Long noncoding RNAs (lncRNAs) are critical regulators of cardiovascular lineage commitment and heart wall development, but their roles in regulating endogenous cardiac regeneration are unclear. The present study investigated the role of human-derived lncRNA in regulating endogenous cardiac regeneration as well as the underlying mechanisms. Methods and results: We compared RNA sequencing data from human foetal and adult hearts and identified a novel lncRNA that was upregulated in adult hearts (Genesymbol NONHSAG000971/NONHSAT002258 or ENST00000497710.5), which was a splice variant of the AZIN2 gene (AZIN2-sv). We used quantitative PCR to confirm the increased expression of AZIN2-sv in adult rat hearts. Coexpression network analysis indicated that AZIN2-sv could regulate proliferation. Loss- and gain-of-function approaches demonstrated that AZIN2-sv negatively regulated endogenous cardiomyocyte proliferation in vitro and in vivo. Knockdown of AZIN2-sv attenuated ventricular remodelling and improved cardiac function after myocardial infarction. Phosphatase and tensin homolog (PTEN) was identified as a target of AZIN2-sv, their direct binding increased PTEN stability. Furthermore, AZIN2-sv acted as a microRNA-214 sponge to release PTEN, which blocked activation of the PI3 kinase/Akt pathway to inhibit cardiomyocyte proliferation. Conclusions: The newly discovered AZIN2-sv suppressed endogenous cardiac regeneration by targeting the PTEN/Akt pathway. Thus, AZIN2-sv may be a novel therapeutic target for preventing and treating heart failure.
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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.