ArticleBioengineered2022
Metformin attenuates high glucose-induced injury in islet microvascular endothelial cells.
Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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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
5 citing papers in PubMed, 7 citations in OpenAlex.
- Empagliflozin improves metabolism and prevents myocardial and coronary dysfunction in streptozotocin-diabetic and non-diabetic rats subjected to ischemia/reperfusion.Basic research in cardiology · 2026Article
- The role of endothelial cells in pancreatic islet development, transplantation and culture.Frontiers in cell and developmental biology · 2025Review
- Overcoming chemoresistance to b-raf inhibitor in melanoma via targeted inhibition of phosphoenolpyruvate carboxykinase1 using 3-mercaptopropionic acid.Bioengineered · 2022Article
- Article
- Pathogenesis and treatment of wound healing in patients with diabetes after tooth extraction.Frontiers in endocrinology · 2022Review
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
As one of the most frequently prescribed antidiabetic drugs, metformin can lower glucose levels, improve insulin resistance manage body weight. However, the effect of metformin on islet microcirculation remains unclear. In the present study, to explore the effect of metformin on islet endothelial cells and investigated the underlying mechanism, we assessed the effects of metformin on islet endothelial cell survival, proliferation, oxidative stress and apoptosis. Our results suggest that metformin stimulates the proliferation of pancreatic islet endothelial cells and inhibits the apoptosis and oxidative stress caused by high glucose levels. By activating farnesoid X receptor (FXR), metformin increases the expression of vascular endothelial growth factor-A (VEGF-A) and endothelial nitric oxide synthase (eNOS), improves the production of nitric oxide (NO) and decreases the production of ROS. After the inhibition of FXR or VEGF-A, all of the effects disappeared. Thus, metformin appears to regulate islet microvascular endothelial cell (IMEC) proliferation, apoptosis and oxidative stress by activating the FXR/VEGF-A/eNOS pathway. These findings provide a new mechanism underlying the islet-protective effect of metformin.
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Registered trials
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