ArticleBioMed research international2020
Overexpression of miR-29a-3p Suppresses Proliferation, Migration, and Invasion of Vascular Smooth Muscle Cells in Atherosclerosis via Targeting TNFRSF1A.
Article in BioMed research international, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
9 citing papers in PubMed, 19 citations in OpenAlex.
- Article
- miR-29a-3p/Renal failure · 2025Article
- Deciphering the role of miRNA-mRNA interactions in cerebral vasospasm post intracranial hemorrhage.Frontiers in molecular biosciences · 2025Article
- Identification of differentially expressed miRNAs involved in vascular aging reveals pathways associated with the endocrine hormone regulation.Biogerontology · 2024Article
- GATA2‑miR‑374a axis promotes vascular smooth muscle cells proliferation, migration via targeting circTADA2A/RORA axis.Experimental and therapeutic medicine · 2024Article
- MicroRNAs Regulate Function in Atherosclerosis and Clinical Implications.Oxidative medicine and cellular longevity · 2023Review
- Article
- Characterization of the microRNA transcriptomes and proteomics of cochlear tissue-derived small extracellular vesicles from mice of different ages after birth.Cellular and molecular life sciences : CMLS · 2022Article
- Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveIncreasing evidence highlights the significance of microRNAs (miRNAs) in the progression of atherosclerosis (AS). Our aim was to probe out the role and regulatory mechanism of miR-29a-3p in AS.
methodsAn in vivo model of AS was conducted by high-fat diet ApoE
resultsUpregulated miR-29a-3p and downregulated TNFRSF1A were found both in vitro and in vivo models of AS. miR-29a-3p mimic distinctly decreased the serum levels of TC, TG, and LDL-C and increased serum HDL-C levels. Moreover, its overexpression could ameliorate plaque formation of AS mice. In ox-LDL-induced VSMCs, miR-29a-3p overexpression notably decreased cell proliferation, migration, and invasion, which was reversed by TNFRSF1A overexpression. Also, miR-29a-3p could directly target the 3'UTR of TNFRSF1A.
conclusionmiR-29a-3p overexpression ameliorated plaque formation of AS and suppressed proliferation, migration, and invasion of ox-LDL-induced VSMCs via TNFRSF1A, which offered novel insights into the progression of AS.
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Registered trials
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