ArticleJournal of cardiovascular translational research2022
MiR-32-3p Regulates Myocardial Injury Induced by Microembolism and Microvascular Obstruction by Targeting RNF13 to Regulate the Stability of Atherosclerotic Plaques.
Article in Journal of cardiovascular translational research, 2022. 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
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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.
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.
- MiR-32-3p improves ISO induced AC16 myocardial cell injury by targeting ATF4.Journal of cardiothoracic surgery · 2026Article
- Role of mir-32-3p in the diagnosis and risk assessment of osteoporotic fractures.Journal of orthopaedic surgery and research · 2024Article
- Integrating machine learning and single-cell transcriptomic analysis to identify potential biomarkers and analyze immune features of ischemic stroke.Scientific reports · 2024Article
- Crosstalk between ubiquitin ligases and ncRNAs drives cardiovascular disease progression.Frontiers in immunology · 2024Review
- Article
- Relationships between Indicators of Lower Extremity Artery Disease and miRNA Expression in Peripheral Blood Mononuclear Cells.Journal of clinical medicine · 2022Article
- MicroRNA Alterations Induced in Human Skin by Diesel Fumes, Ozone, and UV Radiation.Journal of personalized medicine · 2022Article
- FromCells · 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
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study aimed to explore the molecular mechanism of myocardial protection. The effects of miR-32-3p and ring finger protein 13 (RNF13) on endoplasmic reticulum (ER) stress-induced apoptosis of A-10 cells and human umbilical vein endothelial cells (HUVEC) were detected using flow cytometry. The effects of miR-32-3p and phenylbutyric acid (PBA) on plaque instability and myocardial tissue injury in rats were investigated after establishment of arterial plaque model and embolization model and treatment with miR-32-3p-antagomir and PBA. RNF13, which was differentially expressed in myocardial infarction, was the direct target gene of miR-32-3p. MiR-32-3p inhibited RNF13 expression and targeted RNF13 to inhibit ER stress-induced cell apoptosis. Furthermore, inhibiting miR-32-3p expression induced arterial plaque instability by reducing survival, increasing pathological lesions in arterial tissue, up-regulating ER stress-related proteins, and regulating the expressions of apoptosis-related proteins in the model rats. However, PBA reversed the effects of miR-32-3p-antagomir on the model rats. MiR-32-3p regulates myocardial injury induced by micro-embolism and micro-vascular obstruction by targeting RNF13 to regulate the stability of atherosclerotic plaques.
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.