ArticleAtherosclerosis2022
Endothelial cell-specific deletion of a microRNA accelerates atherosclerosis.
Article in Atherosclerosis, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed, 17 citations in OpenAlex.
- TheNon-coding RNA · 2025Article
- LncRNA MIR181A1HG Deficiency Attenuates Vascular Inflammation and Atherosclerosis.Circulation research · 2025Article
- Micro RNA-175 TargetsGenes · 2024Article
- Review
- Roles and Mechanisms of miRNAs in Abdominal Aortic Aneurysm: Signaling Pathways and Clinical Insights.Current atherosclerosis reports · 2024Review
- MicroRNA-181 in cardiovascular disease: Emerging biomarkers and therapeutic targets.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Review
- miR-181b regulates vascular endothelial aging by modulating an MAP3K3 signaling pathway.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022Article
Corrections and comments
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Authors and funding
14 authors at 5 institutions in 2 countries.
Funding
Abstract
BACKGROUND AND
aimsChronic vascular endothelial inflammation predisposes to atherosclerosis; however, the cell-autonomous roles for endothelial-expressing microRNAs (miRNAs) are poorly understood in this process. MiR-181b is expressed in several cellular constituents relevant to lesion formation. The aim of this study is to examine the role of genetic deficiency of the miR-181b locus in endothelial cells during atherogenesis. METHODS AND
resultsUsing a proprotein convertase subtilisin/kexin type 9 (PCSK9)-induced atherosclerosis mouse model, we demonstrated that endothelial cell (EC)-specific deletion of miR-181a2b2 significantly promoted atherosclerotic lesion formation, cell adhesion molecule expression, and the influx of lesional macrophages in the vessel wall. Yet, endothelium deletion of miR-181a2b2 did not affect body weight, lipid metabolism, anti-inflammatory Ly6C
conclusionsOur study establishes that deficiency of a miRNA specifically in the vascular endothelium is sufficient to profoundly impact atherogenesis. Endothelial miR-181a2b2 deficiency regulates multiple key pathways related to endothelial inflammation, cell adhesion, cell cycle, and immune response involved in the development of atherosclerosis.
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Registered trials
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