ArticleFrontiers in physiology2022
Enhanced RAGE Expression and Excess Reactive-Oxygen Species Production Mediates Rho Kinase-Dependent Detrusor Overactivity After Methylglyoxal Exposure.
Article in Frontiers in physiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 21 citations in OpenAlex.
- Elucidating the Urothelial-Dependent and -Independent Mechanisms Involved in the Mouse Bladder Contractility Alterations by Acute Methylglyoxal Exposure.Biomedicines · 2026Article
- Activation of TRPA1 and TRPM3 triggers CaThe Journal of physiology · 2025Article
- The RAGE Inhibitor TTP488 (Azeliragon) Improves Diabetic Bladder Dysfunction in Leptin-Deficient Obese Mice.Antioxidants (Basel, Switzerland) · 2025Article
- Oral bacterium contributes to periodontal inflammation by forming advanced glycation end products.Infection and immunity · 2025Article
- Trehalose induces bladder smooth muscle hypercontractility in mice: involvement of oxidative stress and cellular senescence.Frontiers in physiology · 2025Article
- Diabetic Glycation of Human Serum Albumin Affects Its Immunogenicity.Biomolecules · 2024Article
- Methylglyoxal and Advanced Glycation End Products (AGEs): Targets for the Prevention and Treatment of Diabetes-Associated Bladder Dysfunction?Biomedicines · 2024Review
- Effector function and neutrophil cell death in the severity of sepsis with diabetes mellitus.Narra J · 2024Review
- Alu antisense RNA ameliorates methylglyoxal-induced human lens epithelial cell apoptosis by enhancing antioxidant defense.International journal of ophthalmology · 2023Article
- Selective Pharmacological Inhibition of NOX2 by GSK2795039 Improves Bladder Dysfunction in Cyclophosphamide-Induced Cystitis in Mice.Antioxidants (Basel, Switzerland) · 2022Article
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
Methylglyoxal (MGO) is a highly reactive dicarbonyl compound implicated in diabetes-associated diseases. In vascular tissues, MGO induces the formation of advanced glycation end products (AGEs) that bounds its receptor RAGE, initiating the downstream tissue injury. Outside the cardiovascular system, MGO intake produces mouse voiding dysfunction and bladder overactivity. We have sought that MGO-induced bladder overactivity is due to activation of AGE-RAGE-reactive-oxygen species (ROS) signaling cascade, leading to Rho kinase activation. Therefore, female mice received 0.5% MGO orally for 12 weeks, after which
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