ArticleExperimental and therapeutic medicine2019
High glucose induces apoptosis of HUVECs in a mitochondria-dependent manner by suppressing hexokinase 2 expression.
Article in Experimental and therapeutic medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 24 citations in OpenAlex.
- Phytoextract-loaded bioinspired PLGA nanofibrous scaffold promotes diabetic wound healing via anti-inflammatory and antioxidant effects in in vitro and in vivo experimental models.Journal of molecular histology · 2026Article
- Investigation of Spexin Effects on Insulin-Dependent Pathway Genes in High-Glucose-Induced Insulin-Resistant C2C12 Myotubes.FASEB bioAdvances · 2026Article
- Levels and Effects of Nogo-B in Patients With Type 2 Diabetes or Hyperglycemic HUVEC Model.Endocrinology, diabetes & metabolism · 2026Article
- Glycometabolic Regulation of Angiogenesis: Mechanisms and Therapeutic Strategies.International journal of molecular sciences · 2025Review
- Microfluidic investigation for shear-stress-mediated repair of dysglycemia-induced endothelial cell damage.Mechanobiology in medicine · 2024Review
- Mitochondrial Dysfunction in Endothelial Progenitor Cells: Unraveling Insights from Vascular Endothelial Cells.Biology · 2024Review
- Role of glucose metabolism in ocular angiogenesis (Review).Molecular medicine reports · 2022Review
- Multi-omics study identifies novel signatures of DNA/RNA, amino acid, peptide, and lipid metabolism by simulated diabetes on coronary endothelial cells.Scientific reports · 2022Article
- Combined exposure to fine particulate matter and high glucose aggravates endothelial damage by increasing inflammation and mitophagy: the involvement of vitamin D.Particle and fibre toxicology · 2022Article
- How Do Hexokinases Inhibit Receptor-Mediated Apoptosis?Biology · 2022Review
- The glycolytic process in endothelial cells and its implications.Acta pharmacologica Sinica · 2022Review
- Long term high glucose exposure induces premature senescence in retinal endothelial cells.Frontiers in physiology · 2022Article
- High Glucose Activates YAP Signaling to Promote Vascular Inflammation.Frontiers in physiology · 2021Article
- Antioxidative Potentials of Incretin-Based Medications: A Review of Molecular Mechanisms.Oxidative medicine and cellular longevity · 2021Review
- Article
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
Hyperglycemia in patients with diabetes induces vascular endothelial cell apoptosis and subsequent vasculopathy. The aim of the current study was to investigate the pathological mechanism of hyperglycemia-induced endothelial cell apoptosis and vasculopathy using human umbilical vein endothelial cells. As high glucose-induced apoptosis is caused by elevated mitochondrial permeability-mediated release of mitochondrial cytochrome c, the current study examined voltage-dependent anion channel (VDAC1), the controller of mitochondrial permeability, and its regulators, hexokinase2 (HK2), Bcl-2 and Bax. The current study demonstrated that HK2 may be involved in high glucose-induced cell apoptosis, as HK2 overexpression partially reversed high glucose-induced downregulation of mitochondrial/cellular HK2 and Bcl-2 as well as upregulation of mitochondrial Bax. These results suggest that HK2 overexpression partially reversed the reduced binding of HK2 and Bcl-2 and the enhanced binding of Bax to VDAC1, which reduced the high mitochondrial permeability observed under high-glucose conditions. Furthermore, high glucose reduced HK2 transcription via down-regulation of the HK2 transcriptional factor, peroxisome proliferator activated receptor γ (PPARγ). Taken together, these results suggest that PPARγ/HK2 may be novel targets for the prevention of diabetic vasculopathy.
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