ArticleDiabetes2012
Vascular endothelial growth factor-mediated islet hypervascularization and inflammation contribute to progressive reduction of β-cell mass.
Article in Diabetes, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 86 citations in OpenAlex.
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- Sodium tungstate promotes vascularization to support beta cell replacement in diabetes.EMBO molecular medicine · 2026Article
- The paracrine signalling between endothelial and pancreatic β-cells: implications for oxidative stress and diabetes.Journal of endocrinological investigation · 2026Review
- Preservation of pancreatic endocrine and peri-islet exocrine capillary networks in type 2 diabetes.JCI insight · 2026Article
- Diet-induced obesity promotes endothelial cell desensitization to VEGF-A and permanent islet vessel dysfunction in mice.The Journal of clinical investigation · 2025Article
- Vascular endothelial growth factor signaling in health and disease: from molecular mechanisms to therapeutic perspectives.Signal transduction and targeted therapy · 2025Review
- Neurophysiological mechanisms of electroacupuncture in regulating pancreatic function and adipose tissue expansion.World journal of diabetes · 2025Article
- Application of Ultrasound Localization Microscopy in Evaluating the Type 2 Diabetes Progression.Cyborg and bionic systems (Washington, D.C.) · 2025Article
- Long-term effects of gestational diabetes mellitus on the pancreas of female mouse offspring.World journal of diabetes · 2024Article
- A vascularized 3D model of the human pancreatic islet forBiofabrication · 2024Article
- Toceranib phosphate (Palladia) reverses type 1 diabetes by preserving islet function in mice.The Journal of veterinary medical science · 2023Article
- Serum VEGF as a predictive marker of glycemic control and diabetic nephropathy in Chinese older adults with type 2 diabetes mellitus.Frontiers in endocrinology · 2023Article
- Increased serum cystatin C levels and responses of pancreatic α- and β-cells in type 2 diabetes.Endocrine connections · 2022Article
- Loss of Function of WFS1 Causes ER Stress-Mediated Inflammation in Pancreatic Beta-Cells.Frontiers in endocrinology · 2022Article
- Islet Inflammation and β Cell Dysfunction in Type 2 Diabetes.Handbook of experimental pharmacology · 2022Review
- Physiological Changes and Pathological Pain Associated with Sedentary Lifestyle-Induced Body Systems Fat Accumulation and Their Modulation by Physical Exercise.International journal of environmental research and public health · 2021Review
- Beta cell dysfunction in diabetes: the islet microenvironment as an unusual suspect.Diabetologia · 2020Review
- Islet pericytes convert into profibrotic myofibroblasts in a mouse model of islet vascular fibrosis.Diabetologia · 2020Article
- VEGF-A and blood vessels: a beta cell perspective.Diabetologia · 2019Review
- Engineering the vasculature for islet transplantation.Acta biomaterialia · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Type 2 diabetes (T2D) results from insulin resistance and inadequate insulin secretion. Insulin resistance initially causes compensatory islet hyperplasia that progresses to islet disorganization and altered vascularization, inflammation, and, finally, decreased functional β-cell mass and hyperglycemia. The precise mechanism(s) underlying β-cell failure remain to be elucidated. In this study, we show that in insulin-resistant high-fat diet-fed mice, the enhanced islet vascularization and inflammation was parallel to an increased expression of vascular endothelial growth factor A (VEGF). To elucidate the role of VEGF in these processes, we have genetically engineered β-cells to overexpress VEGF (in transgenic mice or after adeno-associated viral vector-mediated gene transfer). We found that sustained increases in β-cell VEGF levels led to disorganized, hypervascularized, and fibrotic islets, progressive macrophage infiltration, and proinflammatory cytokine production, including tumor necrosis factor-α and interleukin-1β. This resulted in impaired insulin secretion, decreased β-cell mass, and hyperglycemia with age. These results indicate that sustained VEGF upregulation may participate in the initiation of a process leading to β-cell failure and further suggest that compensatory islet hyperplasia and hypervascularization may contribute to progressive inflammation and β-cell mass loss during T2D.
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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 Socratic graph.