ArticleOxidative medicine and cellular longevity2015
Hydrogen Sulfide Prevents Advanced Glycation End-Products Induced Activation of the Epithelial Sodium Channel.
Article in Oxidative medicine and cellular longevity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 21 citations in OpenAlex.
- The dual role of ion channels in diabetic kidney disease: a translational paradigm for biomarkers and target discovery - reviews and prospects.American journal of translational research · 2026Review
- Chemoprotective Mechanism of Sodium Thiosulfate Against Cisplatin-Induced Nephrotoxicity Is via Renal Hydrogen Sulfide, Arginine/cAMP and NO/cGMP Signaling Pathways.International journal of molecular sciences · 2025Article
- NaHS or Lovastatin Attenuates Cyclosporine A-Induced Hypertension in Rats by Inhibiting Epithelial Sodium Channels.Frontiers in pharmacology · 2021Article
- Hydrogen Sulfide Upregulates Acid-sensing Ion ChannelsFunction (Oxford, England) · 2021Article
- An Updated Insight Into Molecular Mechanism of Hydrogen Sulfide in Cardiomyopathy and Myocardial Ischemia/Reperfusion Injury Under Diabetes.Frontiers in pharmacology · 2021Review
- Roles of Hydrogen Sulfide Donors in Common Kidney Diseases.Frontiers in pharmacology · 2020Review
- Effects of reactive oxygen species on renal tubular transport.American journal of physiology. Renal physiology · 2019Review
- Ion channels and transporters in diabetic kidney disease.Current topics in membranes · 2019Review
- Palmitate Stimulates the Epithelial Sodium Channel by Elevating Intracellular Calcium, Reactive Oxygen Species, and Phosphoinositide 3-Kinase Activity.Oxidative medicine and cellular longevity · 2018Article
- Hydrogen peroxide suppresses TRPM4 trafficking to the apical membrane in mouse cortical collecting duct principal cells.American journal of physiology. Renal physiology · 2016Article
- Epithelial Electrolyte Transport Physiology and the Gasotransmitter Hydrogen Sulfide.Oxidative medicine and cellular longevity · 2016Review
- The Role of Hydrogen Sulfide in Renal System.Frontiers in pharmacology · 2016Review
- Hydrogen sulfide therapy: a narrative overview of current research and possible therapeutic implications in future.Medical gas researchReview
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
Abstract
Advanced glycation end-products (AGEs) are complex and heterogeneous compounds implicated in diabetes. Sodium reabsorption through the epithelial sodium channel (ENaC) at the distal nephron plays an important role in diabetic hypertension. Here, we report that H2S antagonizes AGEs-induced ENaC activation in A6 cells. ENaC open probability (P O ) in A6 cells was significantly increased by exogenous AGEs and that this AGEs-induced ENaC activity was abolished by NaHS (a donor of H2S) and TEMPOL. Incubating A6 cells with the catalase inhibitor 3-aminotriazole (3-AT) mimicked the effects of AGEs on ENaC activity, but did not induce any additive effect. We found that the expression levels of catalase were significantly reduced by AGEs and both AGEs and 3-AT facilitated ROS uptake in A6 cells, which were significantly inhibited by NaHS. The specific PTEN and PI3K inhibitors, BPV(pic) and LY294002, influence ENaC activity in AGEs-pretreated A6 cells. Moreover, after removal of AGEs from AGEs-pretreated A6 cells for 72 hours, ENaC P O remained at a high level, suggesting that an AGEs-related "metabolic memory" may be involved in sodium homeostasis. Our data, for the first time, show that H2S prevents AGEs-induced ENaC activation by targeting the ROS/PI3K/PTEN pathway.
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