ArticleJournal of cellular and molecular medicine2018
MicroRNA-216a induces endothelial senescence and inflammation via Smad3/IκBα pathway.
Article in Journal of cellular and molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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.
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Who cites it
37 citing papers in PubMed, 55 citations in OpenAlex.
- Inflammatory cytokines and immune signalling in heart failure: mechanisms, models, and emerging therapies.Cardiovascular research · 2026Review
- Molecular mechanisms and recent advances in cellular senescence.Cell & bioscience · 2026Review
- Review
- The emerging role of miRNAs in biological aging and age-related diseases.Non-coding RNA research · 2025Review
- Regulation of endothelial cell senescence via the miR-217/FOXO3 axis.Biogerontology · 2025Article
- Global Perspectives on Coronary Artery Disease: The Emerging Role of miRNAs.Current atherosclerosis reports · 2025Review
- Circulating microRNAs in Carotid Atherosclerosis: Complex Interplay and Possible Associations with Atherothrombotic Stroke.International journal of molecular sciences · 2024Article
- miRNA-142-3p aggravates hydrogen peroxide-induced human umbilical vein endothelial cell premature senescence by targeting SIRT1.Bioscience reports · 2024Article
- Noncoding RNAs in atherosclerosis: regulation and therapeutic potential.Molecular and cellular biochemistry · 2024Review
- Curcumin improves atrial fibrillation susceptibility by regulating tsRNA expression in aging mouse atrium.PeerJ · 2024Article
- Iron overload induces cerebral endothelial senescence in aged mice and in primary culture in a sex-dependent manner.Aging cell · 2023Article
- Article
- MicroRNA-216a is essential for cardiac angiogenesis.Molecular therapy : the journal of the American Society of Gene Therapy · 2023Article
- Epigenetic modifications as therapeutic targets in atherosclerosis: a focus on DNA methylation and non-coding RNAs.Frontiers in cardiovascular medicine · 2023Review
- Research Progress and Molecular Mechanisms of Endothelial Cells Inflammation in Vascular-Related Diseases.Journal of inflammation research · 2023Review
- Differential Expression of Vascular-Related MicroRNA in Circulating Endothelial Microvesicles in Adults With Spinal Cord Injury: A Pilot Study.Topics in spinal cord injury rehabilitation · 2023Article
- miR-1183 Is a Key Marker of Remodeling upon Stretch and Tachycardia in Human Myocardium.International journal of molecular sciences · 2022Article
- Novel Biomarkers of Atherosclerotic Vascular Disease-Latest Insights in the Research Field.International journal of molecular sciences · 2022Review
- Pathophysiology of Atherosclerosis.International journal of molecular sciences · 2022Review
- TXNIP: A Double-Edged Sword in Disease and Therapeutic Outlook.Oxidative medicine and cellular longevity · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Vascular endothelial senescence contributes to atherosclerosis and coronary artery disease (CAD), but the mechanisms are yet to be clarified. We identified that microRNA-216a (miR-216a) significantly increased in senescent endothelial cells. The replicative senescence model of human umbilical vein endothelial cells (HUVECs) was established to explore the role of miR-216a in endothelial ageing and dysfunction. Luciferase assay indicated that Smad3 was a direct target of miR-216a. Stable expression of miR-216a induced a premature senescence-like phenotype in HUVECs with an impairment in proliferation and migration and led to an increased adhesion to monocytes by inhibiting Smad3 expression and thereafter modulating the degradation of NF-κB inhibitor alpha (IκBα) and activation of adhesion molecules. Conversely, inhibition of endogenous miR-216a in senescent HUVECs rescued Smad3 and IκBα expression and inhibited monocytes attachment. Plasma miR-216a was significantly higher in old CAD patients (>50 years) and associated with increased 31% risk for CAD (odds ratio 1.31, 95% confidence interval 1.03-1.66; P = .03) compared with the matched healthy controls (>50 years). Taken together, our data suggested that miR-216a promotes endothelial senescence and inflammation as an endogenous inhibitor of Smad3/IκBα pathway, which might serve as a novel target for ageing-related atherosclerotic diseases.
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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.