ArticleAnnals of translational medicine2019
High-glucose treatment regulates biological functions of human umbilical vein endothelial cells via Sirt1/FOXO3 pathway.
Article in Annals of translational medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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16 citing papers in PubMed, 19 citations in OpenAlex.
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- Stem cell-derived exosomes from human exfoliated deciduous teeth promote angiogenesis in hyperglycemic-induced human umbilical vein endothelial cells.Journal of applied oral science : revista FOB · 2023Article
- CircRNA-miRNA interactions in atherogenesis.Molecular and cellular biochemistry · 2022Review
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- Aquaporin-8 overexpression is involved in vascular structure and function changes in placentas of gestational diabetes mellitus patients.Open life sciences · 2022Article
- Vitamin D Prevents High Glucose-Induced Lipid Droplets Accumulation in Cultured Endothelial Cells: The Role of Thioredoxin Interacting Protein.Biomedicines · 2021Article
- Metformin alleviates bevacizumab-induced vascular endothelial injury by up-regulating GDF15 and activating the PI3K/AKT/FOXO/PPARγ signaling pathway.Annals of translational medicine · 2021Article
- Endothelial cells from umbilical cord of women affected by gestational diabetes: A suitable in vitro model to study mechanisms of early vascular senescence in diabetes.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
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- Longevity Factor FOXO3: A Key Regulator in Aging-Related Vascular Diseases.Frontiers in cardiovascular medicine · 2021Review
- LncRNA HCG11/miR-26b-5p/QKI5 feedback loop reversed high glucose-induced proliferation and angiogenesis inhibition of HUVECs.Journal of cellular and molecular medicine · 2020Article
- hsa_circ_0058092 protects against hyperglycemia‑induced endothelial progenitor cell damage via miR‑217/FOXO3.International journal of molecular medicine · 2020Article
- Dysregulation of miR-210 is involved in the development of diabetic retinopathy and serves a regulatory role in retinal vascular endothelial cell proliferation.European journal of medical research · 2020Article
- Combination ofEvidence-based complementary and alternative medicine : eCAM · 2020Review
- Roles of Endovascular Calyx Related Enzymes in Endothelial Dysfunction and Diabetic Vascular Complications.Frontiers in pharmacology · 2020Article
- SIRT1-Dependent Upregulation of Antiglycative Defense in HUVECs Is Essential for Resveratrol Protection against High Glucose Stress.Antioxidants (Basel, Switzerland) · 2019Article
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5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHyperglycaemia-induced angiogenesis plays an important role in diabetic retinopathy (DR). This study aimed to investigate the role of sirtuin1 (Sirt1)/forkhead box O3 (FOXO3) pathway in the effects of high-glucose on human umbilical vein endothelial cells (HUVECs).
methodsHUVECs were divided into normal control group (5 mM glucose), high glucose group (30 mM), 30 mM glucose + shsirt1 group, 30 mM glucose + Sirt1 over-expression group (30 mM + Sirt1), 30 mM glucose + Sirt1 agonist SRT group, 30 mM glucose + SRT + FOXO3 silencing group (30 mM + SRT + siFOXO3). Cell proliferation, migration, invasion and apoptosis were determined.
resultsHigh glucose treatment reduced the expression of Sirt1 and FOXO3 in HUVECs. However, Sirt1 over-expression or SRT attenuated the high-glucose-induced inhibition of HUVEC proliferation and migration as well as reduced their apoptosis. In contrast, Sirt1 silencing deteriorated the high-glucose induced inhibition of HUVEC proliferation and migration and further increased HUVEC apoptosis. FOXO3 expression increased with the increase in Sirt1 expression, which was accompanied by enhanced cellular functions. These were abolished after FOXO3 silencing. In addition, Sirt1/FOXO3 regulated HUVEC activities via peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α).
conclusionsSirt1/FOXO3 pathway is essential for the survival of endothelial cells under high-glucose and plays an important role in the development of diabetes-induced retinal vascular endothelial injury.
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