ArticleToxins2022
Methylglyoxal Induces Inflammation, Metabolic Modulation and Oxidative Stress in Myoblast Cells.
Article in Toxins, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
17 citing papers in PubMed, 24 citations in OpenAlex.
- Article
- Indole-2-carboxylic Acid Nanoemulsions: A Novel Approach for Topical Cosmeceuticals with Antioxidant Properties in Human Skin Models.ACS omega · 2026Article
- Microbiota and Methylglyoxal-Derived AGEs: Implications in Ageing and Age-Related Disease.Life (Basel, Switzerland) · 2026Review
- Effects of α-dicarbonyl Compounds on the Differentiation of Chicken Embryonic Myoblasts.The journal of poultry science · 2026Article
- The current clinical management of muscle wasting in hemodialysis patients with end-stage renal disease.International urology and nephrology · 2025Review
- Diet-Derived Advanced Glycation End-Products (AGEs) Induce Muscle Wasting In Vitro, and a StandardizedAntioxidants (Basel, Switzerland) · 2025Article
- The SGLT2 Inhibitor Empagliflozin Mitigates the Harmful Effects of Methylglyoxal Exposure on Ovalbumin-Induced Mouse Airway Inflammation.International journal of molecular sciences · 2025Article
- Vanillin Enhances Photobiomodulation Wound Healing by Modulating Glyco-Oxidative Stress and Glucose Dysmetabolism in Diabetic Wounded Fibroblast Cells.Journal of cellular and molecular medicine · 2025Article
- Combating chronic kidney disease-associated cachexia: A literature review of recent therapeutic approaches.BMC nephrology · 2025Review
- Hemodialysis employing molecular hydrogen (HScientific reports · 2025Article
- Association between triglyceride-glucose index and sarcopenia in patients with chronic kidney disease.Frontiers in endocrinology · 2025Article
- Fibrinogen glycosylation and glycation: molecular insights into thrombosis and vascular disease.Frontiers in molecular biosciences · 2025Review
- An integrated proteomics and metabolomics analysis of methylglyoxal-induced neurotoxicity in a human neuroblastoma cell line.NPJ science of food · 2024Article
- Integrating Genome-Scale Metabolic Models with Patient Plasma Metabolome to Study Endothelial Metabolism In Situ.International journal of molecular sciences · 2024Article
- Aerobic Exercise Ameliorates Muscle Atrophy Induced by MethylglyoxalBiomolecules & therapeutics · 2023Article
- Clinical features and molecular mechanism of muscle wasting in end stage renal disease.BMB reports · 2023Review
- Methylglyoxal activates transient receptor potential A1/V1 via reactive oxygen species in the spinal dorsal horn.Molecular painArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Uremic sarcopenia is a serious clinical problem associated with physical disability and increased morbidity and mortality. Methylglyoxal (MG) is a highly reactive, dicarbonyl uremic toxin that accumulates in the circulatory system in patients with chronic kidney disease (CKD) and is related to the pathology of uremic sarcopenia. The pathophysiology of uremic sarcopenia is multifactorial; however, the details remain unknown. We investigated the mechanisms of MG-induced muscle atrophy using mouse myoblast C2C12 cells, focusing on intracellular metabolism and mitochondrial injury. We found that one of the causative pathological mechanisms of uremic sarcopenia is metabolic flow change to fatty acid synthesis with MG-induced ATP shortage in myoblasts. Evaluation of cell viability revealed that MG showed toxic effects only in myoblast cells, but not in myotube cells. Expression of mRNA or protein analysis revealed that MG induces muscle atrophy, inflammation, fibrosis, and oxidative stress in myoblast cells. Target metabolomics revealed that MG induces metabolic alterations, such as a reduction in tricarboxylic acid cycle metabolites. In addition, MG induces mitochondrial morphological abnormalities in myoblasts. These changes resulted in the reduction of ATP derived from the mitochondria of myoblast cells. Our results indicate that MG is a pathogenic factor in sarcopenia in CKD.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.