ReviewThe Journal of physiology2018
The role of miRNA regulation in fetal cardiomyocytes, cardiac maturation and the risk of heart disease in adults.
Review in The Journal of physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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
31 citing papers in PubMed, 46 citations in OpenAlex.
- Loss of miR-146a induces cardiomyocyte proliferation after myocardial infarction through targeting Kctd15.Journal of molecular medicine (Berlin, Germany) · 2026Article
- Antenatal betamethasone impairs markers of cardiac development and function in near-term lambs.Experimental physiology · 2026Article
- Elevated cortisol concentration in preterm sheep fetuses impacts heart development.Experimental physiology · 2025Article
- Vitamin D and exercise improve VEGF-B production and IGF-1 levels in diabetic rats: insights the role of miR-1 suppression.Scientific reports · 2025Article
- Bibliometric and visual analysis of miRNAs in heart diseases from 2004 to 2023.Frontiers in cardiovascular medicine · 2025Article
- Cardioprotective mechanism of Qixuan Yijianing formula in Graves' disease mice using miRNA sequencing approach.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2024Article
- Cardiac growth patterns and metabolism before and after birth in swine: Role of miR in proliferation, hypertrophy and metabolism.Journal of molecular and cellular cardiology plus · 2024Article
- DAE-CFR: detecting microRNA-disease associations using deep autoencoder and combined feature representation.BMC bioinformatics · 2024Article
- Cellular signaling modulated by miRNA-3652 in ovarian cancer: unveiling mechanistic pathways for future therapeutic strategies.Cell communication and signaling : CCS · 2023Review
- Sex-specific effects ofJournal of molecular and cellular cardiology plus · 2023Article
- Made in the Womb: Maternal Programming of Offspring Cardiovascular Function by an Obesogenic Womb.Metabolites · 2023Review
- Adapting to a new environment: postnatal maturation of the human cardiomyocyte.The Journal of physiology · 2023Review
- STAT5b is a key effector of NRG-1/ERBB4-mediated myocardial growth.EMBO reports · 2023Article
- A change of heart: understanding the mechanisms regulating cardiac proliferation and metabolism before and after birth.The Journal of physiology · 2023Review
- The Role of ncRNAs in Cardiac Infarction and Regeneration.Journal of cardiovascular development and disease · 2023Review
- Deep sequencing unveils altered cardiac miRNome in congenital heart disease.Molecular genetics and genomics : MGG · 2022Article
- Ultrasound-targeted microbubble destruction (UTMD)-mediated miR-150-5p attenuates oxygen and glucose deprivation-induced cardiomyocyte injury by inhibiting TTC5 expression.Molecular biology reports · 2022Article
- New Tricks with Old Dogs: Computational Identification and Experimental Validation of New miRNA-mRNA Regulation in hiPSC-CMs.Biomedicines · 2022Article
- A Structural View of miRNA Biogenesis and Function.Non-coding RNA · 2022Review
- Challenges and innovation: Disease modeling using human-induced pluripotent stem cell-derived cardiomyocytes.Frontiers in cardiovascular medicine · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Myocardial infarction is a primary contributor towards the global burden of cardiovascular disease. Rather than repairing the existing damage of myocardial infarction, current treatments only address the symptoms of the disease and reducing the risk of a secondary infarction. Cardiac regenerative capacity is dependent on cardiomyocyte proliferation, which concludes soon after birth in humans and precocial species such as sheep. Human fetal cardiac tissue has some ability to repair following tissue damage, whereas a fully matured human heart has minimal capacity for cellular regeneration. This is in contrast to neonatal mice and adult zebrafish hearts, which retain the ability to undergo cardiomyocyte proliferation and can regenerate cardiac tissue after birth. In mice and zebrafish models, microRNAs (miRNAs) have been implicated in the regulation of genes involved in cardiac cell cycle progression and regeneration. However, the significance of miRNA regulation in cardiomyocyte proliferation for humans and other large mammals, where the timing of heart development in relation to birth is similar, remains unclear. miRNAs may be valuable targets for therapies that promote cardiac repair after injury. Therefore, elucidating the role of specific miRNAs in large animals, where heart development closely resembles that of humans, remains vitally important for identifying therapeutic targets that may be translated into clinical practice focused on tissue repair.
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What 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.