ArticleExperimental and therapeutic medicine2021
miR-124 promotes apoptosis and inhibits the proliferation of vessel endothelial cells through P38/MAPK and PI3K/AKT pathways, making it a potential mechanism of vessel endothelial injury in acute myocardial infarction.
Article in Experimental and therapeutic medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
8 citing papers in PubMed, 10 citations in OpenAlex.
- Programmed Cell Death of Endothelial Cells in Ischemic Heart Disease: Mechanism and Potential Cell and Gene Therapeutic Prospects.Bioengineering (Basel, Switzerland) · 2026Review
- Protective role of Tongxinluo in mitigating myocardial fibrosis in mice with acute myocardial infarction via neuregulin-1 upregulation and Inhibition of endothelium-interstitial transition.Journal of molecular histology · 2025Article
- Non-coding RNAs and angiogenesis in cardiovascular diseases: a comprehensive review.Molecular and cellular biochemistry · 2024Review
- MicroRNA-specific therapeutic targets and biomarkers of apoptosis following myocardial ischemia-reperfusion injury.Molecular and cellular biochemistry · 2024Review
- Sensitive fluorescence detection of miRNA-124 in cardiomyocytes under oxidative stress using a nucleic acid probe.Heliyon · 2024Article
- Article
- Response surface optimization of a cardioprotective compound through pharmacosomal drug delivery system: in vivo bioavailability and cardioprotective activity potential.Drug delivery and translational research · 2023Article
- The Role of Epithelial Mesenchymal Transition (EMT) in Pathogenesis of Cardiotoxicity: Diagnostic & Prognostic Approach.Molecular biotechnology · 2023Review
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.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Due to its rapid onset and high rates of fatality, acute myocardial infarction (AMI) has long been one of the most fatal diseases among all types of heart diseases. Therefore, intensive research efforts have been focused on understanding AMI's potential pathogenesis to seek effective treatment options. In the present study, 20 peripheral blood samples were collected from patients with AMI, after which reverse transcription-quantitative PCR analysis revealed that microRNA (miR)-124 levels in the peripheral blood of patients with AMI was significantly elevated compared with that in the control group.
Indexed as
Identifiers
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.