ArticleJournal of cellular and molecular medicine2021
Transforming growth factor-β1 signalling triggers vascular endothelial growth factor resistance and monocyte dysfunction in type 2 diabetes mellitus.
Article in Journal of cellular and molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 14 citations in OpenAlex.
- Efficacy study of juxta-anastomotic stenosis of the arteriovenous fistula via percutaneous transluminal angioplasty with different accesses to the arteries and veins.Frontiers in medicine · 2026Article
- TGF-β1 Is Associated with Left Ventricular Dysfunction.Current issues in molecular biology · 2025Article
- Mechanisms and clinical translation of ICOS/ICOSL signaling pathway blockade in delaying vascular complications of type 2 diabetes.Diabetology & metabolic syndrome · 2025Article
- Multilevel Assessment of Glycemic, Hormonal, and Oxidative Parameters in an Experimental Diabetic Female Rat Model.Biomedicines · 2025Article
- Changes in Serum PDGF-C and TGF-β1 Levels After PCI in Premature Coronary Artery Disease: Combined Predictive Value for MACCE.International journal of general medicine · 2025Article
- Pro- and anti-inflammatory cytokines are the game-changers in childhood obesity-associated metabolic disorders (diabetes and non-alcoholic fatty liver diseases).Reviews in endocrine & metabolic disorders · 2024Review
- TGF-β Isoforms and GDF-15 in the Development and Progression of Atherosclerosis.International journal of molecular sciences · 2024Review
- Glycolysis and beyond in glucose metabolism: exploring pulmonary fibrosis at the metabolic crossroads.Frontiers in endocrinology · 2024Review
- Effects of adipose-derived mesenchymal stem cell conditioned medium on human tenocytes exposed to high glucose.Therapeutic advances in musculoskeletal disease · 2024Article
- Exploration and Clinical Verification of the Blood Co-Expression Genes of Type 2 Diabetes Mellitus and Mild Cognitive Dysfunction in the Elderly.Biomedicines · 2023Article
- Exploration of the hypoglycemic mechanism of Fuzhuan brick tea based on integrating global metabolomics and network pharmacology analysis.Frontiers in molecular biosciences · 2023Article
- Diabetic endothelial microangiopathy and pulmonary dysfunction.Frontiers in endocrinology · 2023Review
- Transforming growth factor-β1 signalling triggers vascular endothelial growth factor resistance and monocyte dysfunction in type 2 diabetes mellitus.Journal of cellular and molecular medicine · 2021Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Type 2 diabetes mellitus (T2DM) leads to monocyte dysfunction associated with atherogenesis and defective arteriogenesis. Transforming growth factor (TGF)-β1, placenta growth factor (PlGF)-1 and vascular endothelial growth factor (VEGF)A play important roles in atherogenesis and arteriogenesis. VEGF-receptor (VEGFR)-mediated monocyte migration is inhibited in T2DM (VEGFA resistance), while TGF-β1-induced monocyte migration is fully functional. Therefore, we hypothesize that TGF-β antagonises the VEGFA responses in human monocytes. We demonstrate that monocytes from T2DM patients have an increased migratory response towards low concentrations of TGF-β1, while PlGF-1/VEGFA responses are mitigated. Mechanistically, this is due to increased expression of type II TGF-β receptor in monocytes under high-glucose conditions and increased expression of soluble (s)VEGFR1, which is known to interfere with VEGFA signalling. VEGFA resistance in monocytes from T2DM patients can be rescued by either experimental down-regulation of TGF-β receptor expression in vitro or by functional blocking of TGF-β signalling using either a TGF-β receptor kinase inhibitor or a TGF-β neutralizing antibody. Our data demonstrate that both T2DM and high-glucose potentiate the TGF-β pathway. TGF-β signalling impairs VEGFR-mediated responses in T2DM monocytes and in this way contributes to mononuclear cell dysfunction, provide novel insights into T2DM vascular dysfunction.
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