ArticleMolecular and cellular biochemistry2014
MicroRNA-492 reverses high glucose-induced insulin resistance in HUVEC cells through targeting resistin.
Article in Molecular and cellular biochemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 43 citations in OpenAlex.
- Exercise in atherosclerosis: its beneficial effects and underlying mechanism.Frontiers in cell and developmental biology · 2025Review
- MiRNA-27a mediates insulin resistance in 3T3-L1 cells through the PPARγ.Molecular and cellular biochemistry · 2022Article
- Marine pollutant exposures and human milk extracellular vesicle-microRNAs in a mother-infant cohort from the Faroe Islands.Environment international · 2022Article
- Ginsenoside Rc Ameliorates Endothelial Insulin Resistance via Upregulation of Angiotensin-Converting Enzyme 2.Frontiers in pharmacology · 2021Article
- Role of miRNAs in the pathogenesis of T2DM, insulin secretion, insulin resistance, and β cell dysfunction: the story so far.Journal of physiology and biochemistry · 2020Review
- Downregulation of miRNA‑328 promotes the angiogenesis of HUVECs by regulating the PIM1 and AKT/mTOR signaling pathway under high glucose and low serum condition.Molecular medicine reports · 2020Article
- miR-450a-5p Eliminates MGO-Induced Insulin Resistance via Targeting CREB.International journal of stem cells · 2020Article
- Exercise Reduces Insulin Resistance in Type 2 Diabetes Mellitus via Mediating the lncRNA MALAT1/MicroRNA-382-3p/Resistin Axis.Molecular therapy. Nucleic acids · 2019Article
- Aerobic Exercise Prevents Insulin Resistance Through the Regulation of miR-492/Resistin Axis in Aortic Endothelium.Journal of cardiovascular translational research · 2018Article
- Effect of Long-Term Exercise Training on lncRNAs Expression in the Vascular Injury of Insulin Resistance.Journal of cardiovascular translational research · 2018Article
- MicroRNA, Proteins, and Metabolites as Novel Biomarkers for Prediabetes, Diabetes, and Related Complications.Frontiers in endocrinology · 2018Review
- Thioredoxin plays a key role in retinal neuropathy prior to endothelial damage in diabetic mice.Oncotarget · 2017Article
- Emerging Roles for MicroRNAs in Diabetic Microvascular Disease: Novel Targets for Therapy.Endocrine reviews · 2017Review
- Insights into the molecular mechanisms of diabetes-induced endothelial dysfunction: focus on oxidative stress and endothelial progenitor cells.Endocrine · 2015Article
- Ganglioside GM1 Contributes to the State of Insulin Resistance in Senescent Human Arterial Endothelial Cells.The Journal of biological chemistry · 2015Article
- The short and long of noncoding sequences in the control of vascular cell phenotypes.Cellular and molecular life sciences : CMLS · 2015Review
- Epigenetic mechanisms of endothelial dysfunction in type 2 diabetes.Clinical epigenetics · 2015Article
- Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The development of atherosclerosis (AS) is a multifactorial process, in which elevated plasma resistin (a key factor leading to insulin resistance) levels play an important role. Emerging evidence indicate that microRNAs (miRNAs) are involved in AS; However, the regulation and function of miRNAs in response to AS remain poorly understood. Our study analyzed the effects of miR-492 on insulin resistance, endothelial activation, and resistin expression in apoE knock-out mice and human umbilical vein endothelial cells after high-glucose treatment and miR-492 mimics transfection. We also investigated the underlying molecular mechanisms. Our results showed that high glucose stress induced a significant decrease in miR-492 expression, with a remarkable upregulation of resistin expression. We then identified resistin as a novel direct target of miR-492 using 3'-UTR luciferase reporter assay. Histopathologic examination demonstrated that upregulation of miR-492 attenuated endothelial cells migration and lipid accumulation induced by high glucose stress. Further investigation demonstrated that the upregulation of p-STAT3, SOCS, and P-selectin activation induced by high glucose stress was attenuated by upregulation of miR-492. Together, our findings indicate that miR-492 contributes to insulin resistance and endothelial dysfunction induced by high glucose, via directly downregulating resistin expression, and involving STAT3 phosphorylation, SOCS, and P-selectin activation.
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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.