ArticleNature medicine2014
MicroRNA-126-5p promotes endothelial proliferation and limits atherosclerosis by suppressing Dlk1.
Article in Nature medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 355 papers.
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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.
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Who cites it
355 citing papers in PubMed, 619 citations in OpenAlex.
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- Extracellular vesicle-mediated mechanisms and therapeutic potential in acute lung injury.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Circulating miR-126 and miR-155 are associated with environmental lead exposure: A translational approach via human biomonitoring and bioinformatic networks.Toxicology reports · 2026Article
- Non-coding RNAs in lipid metabolism and their roles in atherosclerosis.Nature reviews. Cardiology · 2026Review
- SiCmiR Atlas: Single-Cell miRNA Landscape Reveals Hub-miRNA and Network Signatures in Human Cancers.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Hypomethylation of VTRNA2-1 promoter predicts adverse outcomes in peripheral artery disease.Clinical epigenetics · 2026Article
- A Road Map to Understanding Cardiovascular Disease in Diabetes: From the AHA Strategically Focused Research Network in Cardiometabolic Health and Type 2 Diabetes.Circulation research · 2026Review
- Large-Scale Protein Assay Identifies Novel Protein Biomarkers Associated With Arterial Stiffness and Vascular Calcification Measures.International journal of hypertension · 2026Article
- Non-coding RNA-driven cardiovascular immunometabolic reprogramming: from inflammatory endotypes to therapeutic opportunities.Frontiers in cell and developmental biology · 2026Review
- Bridging miRNA Research with Clinical Applications in Cardiovascular Diseases: Advances in Delivery Systems and Therapeutic Strategies.Mini reviews in medicinal chemistry · 2026Review
- Bibliometric analysis of research hotspots and emerging trends in microRNAs and atherosclerosis (2007-2025).Frontiers in cardiovascular medicine · 2026Review
- Diagnostic ultrasound-microbubble therapy promotes wound healing through miR-26b-5p-mediated GSK3β suppression.Scientific reports · 2025Article
- Epigenetic‑ncRNA crosstalk in atherosclerosis: Mechanisms, disease progression and therapeutic potential (Review).International journal of molecular medicine · 2025Review
- Exploring the role of miR-126 in diabetes and its complications: a comprehensive review.Diabetology & metabolic syndrome · 2025Review
- HypoxamiRs: the hidden architects of tissue adaptation in hypoxia.Cell death & disease · 2025Review
- Impacts of systemic milieu on cerebrovascular and brain aging: insights from heterochronic parabiosis, blood exchange, and plasma transfer experiments.GeroScience · 2025Review
- Pathogenic and clinical significance of inflammation-associated MicroRNAs in cardiovascular diseases.Molecular biology reports · 2025Review
295 more citing papers are in PubMed but not listed here.
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Authors and funding
14 authors at 7 institutions in 3 countries.
Funding
Abstract
Atherosclerosis, a hyperlipidemia-induced chronic inflammatory process of the arterial wall, develops preferentially at sites where disturbed laminar flow compromises endothelial cell (EC) function. Here we show that endothelial miR-126-5p maintains a proliferative reserve in ECs through suppression of the Notch1 inhibitor delta-like 1 homolog (Dlk1) and thereby prevents atherosclerotic lesion formation. Endothelial recovery after denudation was impaired in Mir126(-/-) mice because lack of miR-126-5p, but not miR-126-3p, reduced EC proliferation by derepressing Dlk1. At nonpredilection sites, high miR-126-5p levels in endothelial cells confer a proliferative reserve that compensates for the antiproliferative effects of hyperlipidemia, such that atherosclerosis was exacerbated in Mir126(-/-) mice. In contrast, downregulation of miR-126-5p by disturbed flow abrogated EC proliferation at predilection sites in response to hyperlipidemic stress through upregulation of Dlk1 expression. Administration of miR-126-5p rescued EC proliferation at predilection sites and limited atherosclerosis, introducing a potential therapeutic approach.
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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.