ArticleKorean circulation journal2012
Krüppel-like factor 2 suppression by high glucose as a possible mechanism of diabetic vasculopathy.
Article in Korean circulation journal, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 21 citations in OpenAlex.
- Impact of statin therapy on CD40:CD40L signaling: mechanistic insights and therapeutic opportunities.Pharmacological reports : PR · 2025Review
- Genome-Wide Identification of lncRNA and mRNA for Diagnosing Type 2 Diabetes in Saudi Arabia.Pharmacogenomics and personalized medicine · 2023Article
- Heart Failure and Diabetes Mellitus: Dangerous Liaisons.International journal of heart failure · 2022Review
- Cellular crosstalk of glomerular endothelial cells and podocytes in diabetic kidney disease.Journal of cell communication and signaling · 2022Review
- A20/TNFAIP3 Increases ENOS Expression in an ERK5/KLF2-Dependent Manner to Support Endothelial Cell Health in the Face of Inflammation.Frontiers in cardiovascular medicine · 2021Article
- The Role of Epidermal Growth Factor Receptor Family of Receptor Tyrosine Kinases in Mediating Diabetes-Induced Cardiovascular Complications.Frontiers in pharmacology · 2021Review
- Fractionated radiation suppresses Kruppel-like factor 2 pathway to a greater extent than by single exposure to the same total dose.Scientific reports · 2020Article
- COMP-Angiopoietin-1 accelerates muscle regeneration through N-cadherin activation.Scientific reports · 2018Article
- Vascular Adaptation to Exercise in Humans: Role of Hemodynamic Stimuli.Physiological reviews · 2017Review
- Reduced Krüppel-like factor 2 expression may aggravate the endothelial injury of diabetic nephropathy.Kidney international · 2015Article
- Blood pressure regulation VIII: resistance vessel tone and implications for a pro-atherogenic conduit artery endothelial cell phenotype.European journal of applied physiology · 2014Review
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND AND
objectivesEndothelial dysfunction is widely observed in diabetes mellitus, resulting in diabetic vascular complications. Krüppel-like factor 2 (KLF2) is implicated as being a key molecule that maintains endothelial function. We evaluated the expression of KLF2 in endothelial cells cultured in high glucose and investigated its functional implication in a diabetic animal model. SUBJECTS AND
methodsHuman umbilical vein endothelial cells (HUVECs) were cultured in physiologically high glucose (35 mM) condition. The Otsuka Long Evans Tokushima Fatty (OLETF) strain of rat was used as an excellent model of obese type II diabetes, and their lean littermates are Long Evans Tokushima Otsuka (LETO) rats.
resultsIn HUVECs cultured in physiologically high glucose condition, FOXO1 was activated whereas KLF2 and endothelial nitric oxide synthase (eNOS) expression was near completely abolished, which was completely reversed by FOXO1 small interfering ribonucleic acid. In the vessels harvested from the OLETF rats, the animal model of type II diabetes, KLF2 and eNOS expression were found depleted. When vascular remodeling was induced in the left common carotid artery by reduction of blood flow with partial ligation of the distal branches, greater neointimal hypertrophy was observed in OLETF rats compared with the control LETO rats.
conclusionKLF2 suppression in endothelial cells by high glucose is a possible mechanism of diabetic endothelial dysfunction. The strategy of replenishing KLF2 may be effective for preventing diabetic vascular dysfunction.
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