ReviewEJIFCC2019
The role of microRNAs in congenital heart disease.
Review in EJIFCC, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
25 citing papers in PubMed, 34 citations in OpenAlex.
- Genetic drivers of congenital cardiac fibrosis.Communications biology · 2026Review
- Omic-signature of bronchopulmonary dysplasia associated pulmonary hypertension in <1500g-birth-weight-infants with hemodynamically significant intracardiac shunt.Pediatric research · 2025Article
- Review
- Prognostic value of neutrophil-lymphocyte ratio, absolute lymphocyte count, and thrombocyte-lymphocyte ratio in predicting the outcomes of tetralogy of fallot primary repair.Frontiers in cardiovascular medicine · 2025Article
- Sertraline-induced 5-HT dysregulation in mouse cardiomyocytes and the impact on calcium handling.American journal of physiology. Heart and circulatory physiology · 2024Article
- Elevated microRNA-187 causes cardiac endothelial dysplasia to promote congenital heart disease through inhibition of NIPBL.The Journal of clinical investigation · 2024Article
- Myocardial tissue expression of mRNA and preoperative neutrophil-lymphocyte ratio in children undergoing congenital heart surgery.Translational pediatrics · 2024Article
- Association of maternal phthalates exposure and metabolic gene polymorphisms with congenital heart diseases: a multicenter case-control study.BMC pregnancy and childbirth · 2024Article
- Posttranscriptional Regulation by Proteins and Noncoding RNAs.Advances in experimental medicine and biology · 2024Article
- MicroRNA‑378: An important player in cardiovascular diseases (Review).Molecular medicine reports · 2023Review
- Maternal Serum tRNA-Derived Fragments (tRFs) as Potential Candidates for Diagnosis of Fetal Congenital Heart Disease.Journal of cardiovascular development and disease · 2023Article
- Epigenetics in Congenital Heart Disease.Journal of the American Heart Association · 2022Review
- miR-29b-3p Inhibitor Alleviates Hypomethylation-Related Aberrations Through a Feedback Loop Between miR-29b-3p and DNA Methylation in Cardiomyocytes.Frontiers in cell and developmental biology · 2022Article
- Preoperative Neutrophil-Lymphocyte Ratio Can Predict Outcomes for Patients Undergoing Tetralogy of Fallot Repair.Brazilian journal of cardiovascular surgery · 2021Article
- Genetic and epigenetic mechanisms in the development of congenital heart diseases.World journal of pediatric surgery · 2021Review
- Genome-wide analysis of primary microRNA expression using H3K36me3 ChIP-seq data.Computational and structural biotechnology journal · 2021Article
- Potential Roles of MyomiRs in Cardiac Development and Related Diseases.Current cardiology reviews · 2021Review
- Exploring the Role of Maternal Nutritional Epigenetics in Congenital Heart Disease.Current developments in nutrition · 2020Review
- MicroRNA and Cardiovascular DiseasesBalkan medical journal · 2020Article
- The Biomarkers for Acute Myocardial Infarction and Heart Failure.BioMed research international · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Congenital heart diseases (CHDs) are the leading inherited cause of perinatal and infant mortality. CHD refers to structural anomalies of the heart and blood vessels that arise during cardiac development and represents a broad spectrum of malformations, including septal and valve defects, lesions affecting the outflow tract and ventricules. Advanced treatment strategies have greatly improved life expectancy and led to expanded population of adult patients with CHD. Thus, a better understanding of the pathogenesis and molecular mechanisms underlying CHDs is essential to improve the diagnosis and prognosis of patients. The etiology of CHD is largely unknown, genetic and environmental factors may contribute to the disease. In addition to the mutations affecting genomic DNA, epigenetic changes are being increasingly acknowledged as key factors in the development and progression of CHDs. The posttranscriptional regulation of gene expression by microRNAs (miRs) controls the highly complex multi-cell lineage process of cardiac tissue formation. In recent years, multiplex experimental models have provided evidence that changes in expression levels of miRs are associated with human cardiovascular disease, including CHD. The newly described correlations between miRs and heart development suggest the potential importance of miRs as diagnostic markers in human cardiovascular diseases. In the future, more intensive research is likely to be carried out to clarify their contribution to personalized management and treatment of CHD patients. In this paper, we discuss the current knowledge on the causative role of miRs in cardiac development and CHDs.
Indexed as
Identifiers
31263391PMC6599193W2970622000What OpenQuestion holds
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.