ArticleCardiovascular research2014
Inhibition of miR-92a improves re-endothelialization and prevents neointima formation following vascular injury.
Article in Cardiovascular research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
86 citing papers in PubMed, 140 citations in OpenAlex.
- Composite biomaterials of polyelectrolyte complex micelle nanoparticles in hyaluronic acid gels enable local, targeted miR-92a inhibition and enhanced angiogenesis in diabetic wound repair.Journal of controlled release : official journal of the Controlled Release Society · 2026Article
- Kinase regulation of miRNA networks in cardiometabolic disease: emerging pathways to precision therapy.Journal of molecular medicine (Berlin, Germany) · 2026Review
- Non-coding RNAs in lipid metabolism and their roles in atherosclerosis.Nature reviews. Cardiology · 2026Review
- Non-coding RNA-driven cardiovascular immunometabolic reprogramming: from inflammatory endotypes to therapeutic opportunities.Frontiers in cell and developmental biology · 2026Review
- Polyelectrolyte complex micelles embedded in hyaluronic acid gels enable local, targeted miR-92a inhibition to accelerate diabetic wound repair.bioRxiv : the preprint server for biology · 2025Article
- Review
- Article
- Connecting the Dots: How MicroRNAs Link Asthma and Atherosclerosis.International journal of molecular sciences · 2025Review
- Article
- Article
- Review
- The Roles of microRNAs in the Cardiovascular System.International journal of molecular sciences · 2023Review
- Electrostatically assembled wound dressings deliver pro-angiogenic anti-miRs preferentially to endothelial cells.Biomaterials · 2023Article
- A biomechanical view of epigenetic tumor regulation.Journal of biological physics · 2023Review
- Article
- New Insights into the Reparative Angiogenesis after Myocardial Infarction.International journal of molecular sciences · 2023Review
- Role of miRNAs in vascular development.Non-coding RNA research · 2023Review
- Dysregulation of Krüppel-like Factor 2 and Myocyte Enhancer Factor 2D Drive Cardiac Microvascular Inflammation and Dysfunction in Diabetes.International journal of molecular sciences · 2023Article
- Review
- Innate Immunity in Cardiovascular Diseases-Identification of Novel Molecular Players and Targets.Journal of clinical medicine · 2023Review
26 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsMicroRNA (miR)-92a is an important regulator of endothelial proliferation and angiogenesis after ischaemia, but the effects of miR-92a on re-endothelialization and neointimal lesion formation after vascular injury remain elusive. We tested the effects of lowering miR-92a levels using specific locked nucleic acid (LNA)-based antimiRs as well as endothelial-specific knock out of miR-92a on re-endothelialization and neointimal formation after wire-induced injury of the femoral artery in mice. METHODS AND
resultsMiR-92a was significantly up-regulated in neointimal lesions following wire-induced injury. Pre-miR-92a overexpression resulted in repression of the direct miR-92a target genes integrin α5 and sirtuin1, and reduced eNOS expression in vitro. MiR-92a impaired proliferation and migration of endothelial cells but not smooth muscle cells. In vivo, systemic inhibition of miR-92a expression with LNA-modified antisense molecules resulted in a significant acceleration of re-endothelialization of the denuded vessel area. Genetic deletion of miR-92a in Tie2-expressing cells, representing mainly endothelial cells, enhanced re-endothelialization, whereas no phenotype was observed in mice lacking miR-92a expression in haematopoietic cells. The enhanced endothelial recovery was associated with reduced accumulation of leucocytes and inhibition of neointimal formation 21 days after injury and led to the de-repression of the miR-92a targets integrin α5 and sirtuin1.
conclusionOur data indicate that inhibition of endothelial miR-92a attenuates neointimal lesion formation by accelerating re-endothelialization and thus represents a putative novel mechanism to enhance the functional recovery following vascular injury.
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.