ArticleMedical science monitor : international medical journal of experimental and clinical research2016
Underexpression of CACNA1C Caused by Overexpression of microRNA-29a Underlies the Pathogenesis of Atrial Fibrillation.
Article in Medical science monitor : international medical journal of experimental and clinical research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
31 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.
- Progress in research on the role of exosomal miRNAs in the diagnosis and treatment of cardiovascular diseases.Frontiers in genetics · 2022Pooled it
- Incorporating graph representation and mutual attention mechanism for MiRNA-MRNA interaction prediction.Frontiers in genetics · 2025Article
- Article
- Research progress of non-coding RNA in atrial fibrillation.Frontiers in cardiovascular medicine · 2023Review
- Cardiovascular Disease-Associated MicroRNAs as Novel Biomarkers of First-Trimester Screening for Gestational Diabetes Mellitus in the Absence of Other Pregnancy-Related Complications.International journal of molecular sciences · 2022Article
- Leveraging Extracellular Non-coding RNAs to Diagnose and Treat Heart Diseases.Journal of cardiovascular translational research · 2022Review
- Article
- lncRNA KCNQ1OT1 may function as a competitive endogenous RNA in atrial fibrillation by sponging miR‑223‑3p.Molecular medicine reports · 2021Article
- A narrative review of non-coding RNAs in atrial fibrillation: potential therapeutic targets and molecular mechanisms.Annals of translational medicine · 2021Review
- Expanding the phenotype of CACNA1C mutation disorders.Molecular genetics & genomic medicine · 2021Article
- Transcriptome analysis reveals key pathways that vary in patients with paroxysmal and persistent atrial fibrillation.Experimental and therapeutic medicine · 2021Article
- Integrative analysis reveals essential mRNA, long non-coding RNA (lncRNA), and circular RNA (circRNA) in paroxysmal and persistent atrial fibrillation patients.Anatolian journal of cardiology · 2021Article
- Article
- New Insights into the Role of miR-29a in Hepatocellular Carcinoma: Implications in Mechanisms and Theragnostics.Journal of personalized medicine · 2021Review
- Role of Selected miRNAs as Diagnostic and Prognostic Biomarkers in Cardiovascular Diseases, Including Coronary Artery Disease, Myocardial Infarction and Atherosclerosis.Journal of cardiovascular development and disease · 2021Review
- The Role of Exosomes and Their Cargos in the Mechanism, Diagnosis, and Treatment of Atrial Fibrillation.Frontiers in cardiovascular medicine · 2021Review
- The CaMKII phosphorylation site Thr1604 in the CaChannels (Austin, Tex.) · 2020Article
- Genetics and Epigenetics of Atrial Fibrillation.International journal of molecular sciences · 2020Review
- Long Non-Coding RNAs in Atrial Fibrillation: Pluripotent Stem Cell-Derived Cardiomyocytes as a Model System.International journal of molecular sciences · 2020Review
- Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND The objective of this study was to investigate the molecular mechanism of atrial fibrillation (AF), as well as the negative regulatory relationship between miR-29a-3p and CACNA1C. MATERIAL AND METHODS We searched the online miRNA database (www.mirdb.org) and identified the miR-29a-3p binding sequence within the 3'-UTR of the target gene, and then conducted luciferase assay to verify it. The cells were transfected with miR-29a-3p and ICa,L was determined in those cells. RESULTS We validated CACNA1C to be the direct target gene of miR-29a-3p. We also established the negative regulatory relationship between miR-29a-3p and CACNA1C via studying the relative luciferase activity. We also conducted real-time PCR and Western blot analysis to study the mRNA and protein expression level of CACNA1C among different groups of cells treated with scramble control, 30nM miR-29a-3p mimics, and 60nM miR-29a-3p mimics, indicating a negative regulatory relationship between miR-29a-3p and CACNA1C. We next analyzed whether miR-29a-3p transfection in cardiomyocytes produced the effects on the ICa,L induced by electrical remodeling, and found a tonic inhibition of IBa by endogenous miR-29a-3p in atrial myocytes. CONCLUSIONS We validated the negative regulation between miR-29a-3p and CACNA1C, and found that miR-29a-3p might a potential therapeutic target in the treatment of AF.
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Registered trials
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