ArticlePloS one2015
Advanced Glycation End Products Impair Voltage-Gated K+ Channels-Mediated Coronary Vasodilation in Diabetic Rats.
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 12 papers.
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Who cites it
12 citing papers in PubMed, 20 citations in OpenAlex.
- Potassium channels in vascular smooth muscle cells.Physiological reviews · 2026Review
- Established dietary interventions and time-restricted eating for cardiovascular disease prevention.Cell reports. Medicine · 2025Review
- Identification of Potential Therapeutic Targets for Coronary Atherosclerosis from an Inflammatory Perspective Through Integrated Proteomics and Single-Cell Omics.International journal of molecular sciences · 2025Article
- The roles of melatonin and potassium channels in relaxation response to ang 1-7 in diabetic rat isolated aorta.Cytotechnology · 2025Article
- Relationships between advanced glycation end products (AGEs), vasoactive substances, and vascular function.Journal of smooth muscle research = Nihon Heikatsukin Gakkai kikanshi · 2021Article
- Cellular and molecular effects of hyperglycemia on ion channels in vascular smooth muscle.Cellular and molecular life sciences : CMLS · 2021Review
- Role of peroxisome proliferators-activated receptor-gamma in advanced glycation end product-mediated functional loss of voltage-gated potassium channel in rat coronary arteries.BMC cardiovascular disorders · 2020Article
- Mechanisms underlying suppression of noradrenaline-induced contraction by prolonged treatment with advanced glycation end-products in organ-cultured rat carotid artery.Pflugers Archiv : European journal of physiology · 2020Article
- Changes in Myocardial Metabolism Preceding Sudden Cardiac Death.Frontiers in physiology · 2020Review
- Diabetes Mellitus and Ischemic Heart Disease: The Role of Ion Channels.International journal of molecular sciences · 2018Review
- Regulation of voltage-gated potassium channels in vascular smooth muscle during hypertension and metabolic disorders.Microcirculation (New York, N.Y. : 1994) · 2018Review
- Advanced glycation end products impair coronary artery BK channels via AMPK/Akt/FBXO32 signaling pathway.Diabetes & vascular disease researchArticle
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundWe have previously reported that high glucose impairs coronary vasodilation by reducing voltage-gated K+ (Kv) channel activity. However, the underlying mechanisms remain unknown. Advanced glycation end products (AGEs) are potent factors that contribute to the development of diabetic vasculopathy. The aim of this study was to investigate the role of AGEs in high glucose-induced impairment of Kv channels-mediated coronary vasodilation.
methodsPatch-clamp recording and molecular biological techniques were used to assess the function and expression of Kv channels. Vasodilation of isolated rat small coronary arteries was measured using a pressurized myograph. Treatment of isolated coronary vascular smooth muscle cells (VSMCs) and streptozotocin-induced diabetic rats with aminoguanidine, the chemical inhibitor of AGEs formation, was performed to determine the contribution of AGEs.
resultsIncubation of VSMCs with high glucose reduced Kv current density by 60.4 ± 4.8%, and decreased expression of Kv1.2 and Kv1.5 both at the gene and protein level, whereas inhibiting AGEs formation or blocking AGEs interacting with their receptors prevented high glucose-induced impairment of Kv channels. In addition, diabetic rats manifested reduced Kv channels-mediated coronary dilation (9.3 ± 1.4% vs. 36.9 ± 1.4%, P < 0.05), which was partly corrected by the treatment with aminoguanidine (24.4 ± 2.2% vs. 9.3 ± 1.4%, P < 0.05).
conclusionsExcessive formation of AGEs impairs Kv channels in VSMCs, then leading to attenuation of Kv channels-mediated coronary vasodilation.
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