ArticleKorean circulation journal2023
LncRNA AC005332.7 Inhibited Ferroptosis to Alleviate Acute Myocardial Infarction Through Regulating miR-331-3p/CCND2 Axis.
Article in Korean circulation journal, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 22 citations in OpenAlex.
- Clinical value analysis of long non-coding RNA PVT1 in the diagnosis and prognosis, of acute myocardial infarction with arrhythmia.Journal of cardiothoracic surgery · 2026Article
- Ferroptosis in Cardiovascular Diseases and Ferroptosis-Related Intervention Approaches.Cardiovascular drugs and therapy · 2025Review
- Study on the mechanism and clinical value of miR-210-3p and miR-582-5p in acute myocardial infarction by targeting MXD1.Journal of cardiothoracic surgery · 2025Article
- Ferroptosis-related LncRNAs in diseases.BMC biology · 2025Review
- Epigenetic regulation and post-translational modifications of ferroptosis-related factors in cardiovascular diseases.Clinical epigenetics · 2025Review
- Ferroptosis and protein translation: emerging perspectives in the research of myocardial infraction.Frontiers in cardiovascular medicine · 2025Review
- Importance of long non-coding RNAs in the pathogenesis, diagnosis, and treatment of myocardial infarction.International journal of cardiology. Heart & vasculature · 2024Review
- Cardiomyocyte Autophagy: A Novel Therapeutic Target by LncRNA PART1.Korean circulation journal · 2024Article
- Ferroptosis and Lipid Metabolism in Acute Myocardial Infarction.Reviews in cardiovascular medicine · 2024Review
- The interplay of miRNAs and ferroptosis in diseases related to iron overload.Apoptosis : an international journal on programmed cell death · 2024Review
- Construction of the miRNA/Pyroptosis-Related Molecular Regulatory Axis in Abdominal Aortic Aneurysm: Evidence From Transcriptome Data Combined With Multiple Machine Learning Approaches Followed by Experiment Validation.Journal of immunology research · 2024Article
- Ferroptosis and myocardial ischemia-reperfusion: mechanistic insights and new therapeutic perspectives.Frontiers in pharmacology · 2024Review
- Review
- LOXL1-AS1/miR-761/PTEN as a Novel Signaling Pathway in Myocardial Ischemia and Reperfusion Injury (MIRI): Epigenetic Regulation by Long Non-Coding RNA (LncRNA) in MIRI.Korean circulation journal · 2023Article
- The Role of Long Non-Coding RNA (LncRNA) in Acute Myocardial Infarction: Novel Strategy for the Treatment of Acute Myocardial Infarction.Korean circulation journal · 2023Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
BACKGROUND AND
objectivesAcute myocardial infarction (AMI) often occurs suddenly and leads to fatal consequences. Ferroptosis is closely related to the progression of AMI. However, the specific mechanism of ferroptosis in AMI remains unclear.
methodsWe constructed a cell model of AMI using AC16 cells under oxygen and glucose deprivation (OGD) conditions and a mice model of AMI using the left anterior descending (LAD) ligation. The 3-(4, 5-dimethylthiazol-2-yl)-2, 5 diphenyltetrazolium bromide was employed to determine cell viability. The levels of lactate dehydrogenase, creatine kinase, reactive oxygen species (ROS), glutathione (GSH), malondialdehyde (MDA), and iron were measured using corresponding kits. Dual luciferase reporter gene assay, RNA-binding protein immunoprecipitation, and RNA pull-down were performed to validate the correlations among AC005332.7, miR-331-3p, and cyclin D2 (CCND2). Hematoxylin and eosin staining was employed to evaluate myocardial damage.
resultsAC005332.7 and CCND2 were lowly expressed, while miR-331-3p was highly expressed in vivo and in vitro models of AMI. AC005332.7 sufficiency reduced ROS, MDA, iron, and ACSL4 while boosting the GSH and GPX4, indicating that AC005332.7 sufficiency impeded ferroptosis to improve cardiomyocyte injury in AMI. Mechanistically, AC005332.7 interacted with miR-331-3p, and miR-331-3p targeted CCND2. Additionally, miR-331-3p overexpression or CCND2 depletion abolished the suppressive impact of AC005332.7 on ferroptosis in OGD-induced AC16 cells. Moreover, AC005332.7 overexpression suppressed ferroptosis in mice models of AMI.
conclusionsAC005332.7 suppressed ferroptosis in OGD-induced AC16 cells and LAD ligation-operated mice through modulating miR-331-3p/CCND2 axis, thereby mitigating the cardiomyocyte injury in AMI, which proposed novel targets for AMI treatment.
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