ArticlePloS one2015
Intermittent high glucose implements stress-induced senescence in human vascular endothelial cells: role of superoxide production by NADPH oxidase.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
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Who cites it
63 citing papers in PubMed, 114 citations in OpenAlex.
- The paracrine signalling between endothelial and pancreatic β-cells: implications for oxidative stress and diabetes.Journal of endocrinological investigation · 2026Review
- Myovascular Niche: The Role of Endothelial Cells in Skeletal Muscle Health and Disease.Circulation research · 2026Review
- PI3KCD gene expression and its role in diabetic intervertebral disc degeneration running title: PI3KCD gene crucial for diabetic IDH.Mammalian genome : official journal of the International Mammalian Genome Society · 2026Article
- γ-Oryzanol Ameliorates Endothelial Replicative Senescence via Downregulation of SGLT2 Expression to Attenuate NADPH-Driven Oxidative Stress.Biomolecules & therapeutics · 2026Article
- Breaking barriers in pulmonary health of patients with metabolic diseases: senolytics and beyond.Frontiers in aging · 2026Review
- Association between time-weighted average glucose concentration or glucose variability and acute kidney injury among coronary artery disease patients with prediabetes.Renal failure · 2025Article
- The Impact of Glycaemic Variability on Vascular Dysfunction in Diabetes.Biomolecules · 2025Review
- Association between glycemic variability in patients with traumatic lung injury and risk of in-hospital death: a retrospective analysis based on the Medical Information Mart for Intensive Care IV (MIMIC-IV) database.Journal of thoracic disease · 2025Article
- Postprandial metabolic effects of milk and yoghurt in young and older adults.Genes & nutrition · 2025Article
- Hypoglycemia and glycemic variability in acute myocardial infarction: the lesser-known aspects of glycemic control.Cardiovascular diabetology · 2025Review
- The secretome of senescent monocytes predicts age-related clinical outcomes in humans.Nature aging · 2025Article
- Metformin reduces the risk of frailty: evidence from a Mendelian randomization study.Diabetology & metabolic syndrome · 2025Article
- Compression of morbidity by interventions that steepen the survival curve.Nature communications · 2025Article
- Glycemic Variability and Its Association with Traditional Glycemic Control Biomarkers in Patients with Type 1 Diabetes: A Cross-Sectional, Multicenter Study.Journal of clinical medicine · 2025Article
- Mechanisms of cellular senescence-induced vascular aging: evidence of senotherapeutic strategies.The journal of cardiovascular aging · 2025Article
- The senescence-associated secretory phenotype and its physiological and pathological implications.Nature reviews. Molecular cell biology · 2024Review
- Podocyte senescence: from molecular mechanisms to therapeutics.Renal failure · 2024Review
- Microfluidic investigation for shear-stress-mediated repair of dysglycemia-induced endothelial cell damage.Mechanobiology in medicine · 2024Review
- Glycemic variability: Measurement, target, impact on complications of diabetes and does it really matter?Journal of diabetes investigation · 2024Review
- Anti-angiogenic and antioxidant effects of axitinib in human retinal endothelial cells: implications in diabetic retinopathy.Frontiers in pharmacology · 2024Article
3 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Impaired glucose tolerance characterized by postprandial hyperglycemia, which occurs frequently in elderly persons and represents an important preliminary step in diabetes mellitus, poses an independent risk factor for the development of atherosclerosis. Endothelial cellular senescence is reported to precede atherosclerosis. We reported that continuous high glucose stimulus causes endothelial senescence more markedly than hypertension or dyslipidemia stimulus. In the present study, we evaluated the effect of fluctuating glucose levels on human endothelial senescence. Constant high glucose increased senescence-associated-β-galactosidase (SA-β-gal) activity, a widely used marker for cellular senescence. Interestingly, in intermittent high glucose, this effect was more pronounced as well as increase of p21 and p16INK4a , senescence related proteins with DNA damage. However, telomerase was not activated and telomere length was not shortened, thus stress-induced senescence was shown. However, constant high glucose activated telomerase and shortened telomere length, which suggested replicative senescence. Intermittent but not constant high glucose strikingly up-regulated the expression of p22phox, an NADPH oxidase component, increasing superoxide. The small interfering RNA of p22phox undermined the increase in SA-β-gal activity induced by intermittent high glucose. Conclusively, intermittent high glucose can promote vascular endothelial senescence more than constant high glucose, which is in partially dependent on superoxide overproduction.
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