ArticleJournal of clinical laboratory analysis2021
Overexpressed miR-335-5p reduces atherosclerotic vulnerable plaque formation in acute coronary syndrome.
Article in Journal of clinical laboratory analysis, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 26 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.
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Who cites it
26 citing papers in PubMed, 40 citations in OpenAlex.
- miR-330-3p promotes acute coronary syndrome progression via targeting RGS5.Journal of cardiothoracic surgery · 2026Article
- The notch-miR-188-5p-TIMP2/3 axis orchestrates exosome-driven pre-metastatic niche formation in colorectal cancer.Cancer cell international · 2026Article
- Dysregulation of Serum miR-212-3p Serves as a Biomarker to Predict Disease Onset and Short-Term Prognosis in Acute Coronary Syndrome Patients.Anatolian journal of cardiology · 2025Article
- Retraction: Overexpressed miR-335-5p Reduces Atherosclerotic Vulnerable Plaque Formation in Acute Coronary Syndrome.Journal of clinical laboratory analysis · 2025Article
- The Clinical Significance of miR-139-5p in Acute Coronary Syndrome and its Potential Effect on the Progression of Acute Coronary Syndrome.Journal of cardiovascular translational research · 2025Article
- Single-cell transcriptomics of bronchoalveolar lavage during PRRSV infection with different virulence.Nature communications · 2025Article
- Bone marrow mesenchymal stem cell-derived exosomal microRNA-335 alleviates vascular calcification by targeting SP1.Frontiers in cardiovascular medicine · 2025Article
- Identifying the Interaction Between Tuberculosis and SARS-CoV-2 Infections via Bioinformatics Analysis and Machine Learning.Biochemical genetics · 2024Article
- CXCL9, IL2RB, and SPP1, potential diagnostic biomarkers in the co-morbidity pattern of atherosclerosis and non-alcoholic steatohepatitis.Scientific reports · 2024Article
- Two sides of the same coin: Non-alcoholic fatty liver disease and atherosclerosis.Vascular pharmacology · 2024Review
- Longitudinal dynamics of circulating miRNAs in a swine model of familial hypercholesterolemia during early atherosclerosis.Scientific reports · 2023Article
- Characterization of miR-335-5p and miR-335-3p in human osteoarthritic tissues.Arthritis research & therapy · 2023Article
- Associations between circulating microRNAs and lipid-rich coronary plaques measured with near-infrared spectroscopy.Scientific reports · 2023Article
- Screening of Biomarkers Related to Myocardial Infarction Based on the Construction of a ceRNA Regulation Network.Anatolian journal of cardiology · 2023Article
- Properties and fate of human mesenchymal stem cells upon miRNA let-7f-promoted recruitment to atherosclerotic plaques.Cardiovascular research · 2023Article
- Vulnerable Atherosclerotic Plaque: Is There a Molecular Signature?International journal of molecular sciences · 2022Review
- Extracellular vesicles carrying proinflammatory factors may spread atherosclerosis to remote locations.Cellular and molecular life sciences : CMLS · 2022Article
- Long noncoding RNA DANCR expression and its predictive value in patients with atherosclerosis.Bioengineered · 2022Article
- Identification of Key Non-coding RNAs and Transcription Factors in Calcific Aortic Valve Disease.Frontiers in cardiovascular medicine · 2022Article
- Molecular basis of acute coronary syndrome.Journal of research in medical sciences : the official journal of Isfahan University of Medical Sciences · 2022Review
Corrections and comments
- Retracted
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAcute coronary syndrome (ACS) may induce cardiovascular death. The correlation of mast cells related microRNAs (miRs) with risk of ACS has been investigated. We explored regulatory mechanism of miR-335-5p on macrophage innate immune response, atherosclerotic vulnerable plaque formation, and revascularization in ACS in relation to Notch signaling.
methodsACS-related gene microarray was collected from Gene Expression Omnibus database. After different agomir or antagomir, or inhibitor of Notch signaling treatment, IL-6, IL-1β, TNF-α, MCP-1, ICAM-1, and VCAM-1 levels were tested in ACS mice. Additionally, Notch signaling-related genes and matrix metalloproteinases (MMPs) were measured after miR-335-5p interference. Finally, mouse atherosclerosis, lipid accumulation, and the collagen/vessel area ratio of plaque were determined.
resultsmiR-335-5p targeted JAG1 and mediated Notch signaling in ACS. miR-335-5p up-regulation and Notch signaling inhibition reduced expression of JAG1, Notch pathway-related genes, IL-6, IL-1β, TNF-α, MCP-1, ICAM-1, VCAM-1, and MMPs, but promote TIMP1 and TIMP2 expression. Additionally, vulnerable plaques were decreased and collagen fiber contents were observed to increase after miR-335-5p overexpression and Notch signaling inhibition.
conclusionsOverexpression of miR-335-5p inhibited innate immune response of macrophage, reduced atherosclerotic vulnerable plaque formation, and promoted revascularization in ACS mice targeting JAG1 through Notch signaling.
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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.