ArticleMolecular medicine (Cambridge, Mass.)2015
Glucagon-Like Peptide 1 Protects against Hyperglycemic-Induced Endothelial-to-Mesenchymal Transition and Improves Myocardial Dysfunction by Suppressing Poly(ADP-Ribose) Polymerase 1 Activity.
Article in Molecular medicine (Cambridge, Mass.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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23 citing papers in PubMed, 35 citations in OpenAlex.
- Comment on: GLP-1 receptor agonists and male sexual health: translating cardiometabolic benefits into erectile outcomes.International journal of impotence research · 2026Article
- Reprogramming of Mitochondrial and Cellular Energy Metabolism in Fibroblasts and Cardiomyocytes: Mechanisms and Therapeutic Strategies in Cardiac Fibrosis.Journal of cardiovascular translational research · 2025Review
- Atherosclerosis in diabetes mellitus: novel mechanisms and mechanism-based therapeutic approaches.Nature reviews. Cardiology · 2025Review
- Diabetes-Driven Atherosclerosis: Updated Mechanistic Insights and Novel Therapeutic Strategies.International journal of molecular sciences · 2025Review
- The therapeutic effects and mechanisms of glucagon-like peptide-1 receptor agonists in neurocognitive disorders.Therapeutic advances in neurological disorders · 2025Review
- miR-132-3p and KLF7 as novel regulators of aortic stiffening-associated EndMT in type 2 diabetes mellitus.Diabetology & metabolic syndrome · 2023Article
- The Role of NLRP3 Inflammasome in Diabetic Cardiomyopathy and Its Therapeutic Implications.Oxidative medicine and cellular longevity · 2022Review
- Inflammation and Oxidative Stress in Diabetic Kidney Disease: The Targets for SGLT2 Inhibitors and GLP-1 Receptor Agonists.International journal of molecular sciences · 2021Review
- High Glucose Induced Changes in Human VEC Phenotype in a 3D Hydrogel Derived From Cell-Free Native Aortic Root.Frontiers in cardiovascular medicine · 2021Article
- A novel role of kallikrein-related peptidase 8 in the pathogenesis of diabetic cardiac fibrosis.Theranostics · 2021Article
- Endothelial-to-mesenchymal transition in anticancer therapy and normal tissue damage.Experimental & molecular medicine · 2020Review
- Article
- The therapeutic potential of targeting the endothelial-to-mesenchymal transition.Angiogenesis · 2019Review
- Glucagon-like peptide-1 (GLP-1) mediates the protective effects of dipeptidyl peptidase IV inhibition on pulmonary hypertension.Journal of biomedical science · 2019Article
- Natural Plants Compounds as Modulators of Epithelial-to-Mesenchymal Transition.Frontiers in pharmacology · 2019Review
- Endothelial to Mesenchymal Transition Represents a Key Link in the Interaction between Inflammation and Endothelial Dysfunction.Frontiers in immunology · 2018Review
- Prolyl 4-Hydroxylase Domain Protein 3 Overexpression Improved Obstructive Sleep Apnea-Induced Cardiac Perivascular Fibrosis Partially by Suppressing Endothelial-to-Mesenchymal Transition.Journal of the American Heart Association · 2017Article
- Vildagliptin ameliorates pulmonary fibrosis in lipopolysaccharide-induced lung injury by inhibiting endothelial-to-mesenchymal transition.Respiratory research · 2017Article
- Suppression of TAK1 pathway by shear stress counteracts the inflammatory endothelial cell phenotype induced by oxidative stress and TGF-β1.Scientific reports · 2017Article
- Activation of Nrf2 Attenuates Pulmonary Vascular Remodeling via Inhibiting Endothelial-to-Mesenchymal Transition: an Insight from a Plant Polyphenol.International journal of biological sciences · 2017Article
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
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Abstract
Under high glucose conditions, endothelial cells respond by acquiring fibroblast characteristics, that is, endothelial-to-mesenchymal transition (EndMT), contributing to diabetic cardiac fibrosis. Glucagon-like peptide-1 (GLP-1) has cardioprotective properties independent of its glucose-lowering effect. However, the potential mechanism has not been fully clarified. Here we investigated whether GLP-1 inhibits myocardial EndMT in diabetic mice and whether this is mediated by suppressing poly(ADP-ribose) polymerase 1 (PARP-1). Streptozotocin diabetic C57BL/6 mice were treated with or without GLP-1 analog (24 nmol/kg daily) for 24 wks. Transthoracic echocardiography was performed to assess cardiac function. Human aortic endothelial cells (HAECs) were cultured in normal glucose (NG) (5.5 mmol/L) or high glucose (HG) (30 mmol/L) medium with or without GLP-1analog. Immunofluorescent staining and Western blot were performed to evaluate EndMT and PARP-1 activity. Diabetes mellitus attenuated cardiac function and increased cardiac fibrosis. Treatment with the GLP-1 analog improved diabetes mellitus-related cardiac dysfunction and cardiac fibrosis. Immunofluorescence staining revealed that hyperglycemia markedly increased the percentage of von Willebrand factor (vWF)(+)/alpha smooth muscle actin (α-SMA)(+) cells in total α-SMA(+) cells in diabetic hearts compared with controls, which was attenuated by GLP-1 analog treatment. In cultured HAECs, immunofluorescent staining and Western blot also showed that both GLP-1 analog and PARP-1 gene silencing could inhibit the HG-induced EndMT. In addition, GLP-1 analog could attenuate PARP-1 activation by decreasing the level of reactive oxygen species (ROS). Therefore, GLP-1 treatment could protect against the hyperglycemia-induced EndMT and myocardial dysfunction. This effect is mediated, at least partially, by suppressing PARP-1 activation.
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