ArticleAging2021
Resveratrol improves Gly-LDL-induced vascular endothelial cell apoptosis, inflammatory factor secretion and oxidative stress by regulating miR-142-3p and regulating SPRED2-mediated autophagy.
Article in Aging, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- Jingling Granules alleviate atherosclerosis through activating autophagy and inhibiting human umbilical vein endothelial cells apoptosis.Scientific reports · 2026Article
- Comprehensive treatment of diabetic endothelial dysfunction based on pathophysiological mechanism.Frontiers in medicine · 2025Review
- Targeting Autophagy: A Promising Therapeutic Strategy for Diabetes Mellitus and Diabetic Nephropathy.Diabetes therapy : research, treatment and education of diabetes and related disorders · 2024Review
- Traditional Chinese medicine and its active substances reduce vascular injury in diabetes via regulating autophagic activity.Frontiers in pharmacology · 2024Review
- Physiological and pathological characteristics of vascular endothelial injury in diabetes and the regulatory mechanism of autophagy.Frontiers in endocrinology · 2023Review
- Review
- Sprouty-related proteins with EVH1 domain (SPRED2) prevents high-glucose induced endothelial-mesenchymal transition and endothelial injury by suppressing MAPK activation.Bioengineered · 2022Article
- Perturbed autophagy intervenes systemic lupus erythematosus by active ingredients of traditional Chinese medicine.Frontiers in pharmacology · 2022Review
- Article
- Natural Products: A Promising Therapeutics for Targeting Tumor Angiogenesis.Frontiers in oncology · 2021Review
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundResveratrol improves cell apoptosis and tissue damage induced by high glucose, but the specific mechanism is unknown.
methodsThis is a basic research. We performed cell transfection, real-time fluorescence quantitative PCR (qPCR), flow cytometry, immunofluorescence, western blot, enzyme linked immunosorbent assay (ELISA) and cell viability assay to analyze cell viability, cell cycle, cellular oxidative stress, intracellular inflammatory factors and autophagy activities
resultsResveratrol inhibited the expression of miR-142-3p in human umbilical vein endothelial cells (HUVECs) induced by Gly-LDL in a dose-dependent manner, and the overexpression of miR-142-3p reverses the effect of resveratrol on the proliferation, apoptosis, secretion of inflammatory factors, oxidative stress, and autophagy. The dual-luciferase report analysis found a negative regulatory relationship between miR-142-3p and SPRED2. Inhibition of SPRED2 reversed the effects of resveratrol on Gly-LDL-induced HUVECs proliferation, apoptosis, inflammatory factor secretion and oxidative stress, and reversed the effects of resveratrol on Gly-LDL-induced HUVECs autophagy.
conclusionmiR-142-3p promotes the development of diabetes by inhibiting SPRED2-mediated autophagy, including inducing cell apoptosis, aggravating cellular oxidative stress and secretion of inflammatory factors, and resveratrol improves this effect.
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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.