ArticleScientific reports2021
Deletion of RAGE fails to prevent hepatosteatosis in obese mice due to impairment of other AGEs receptors and detoxifying systems.
Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- RAGE Is Essential for Subretinal Fibrosis in Laser-Induced Choroidal Neovascularization: Therapeutic Implications.Investigative ophthalmology & visual science · 2025Article
- Pyridoxamine reduces inflammatory and microcirculatory abnormalities in metabolic dysfunction-associated steatohepatitis and modulates key factors in the hepatic AGE/ALE signaling pathway.Frontiers in physiology · 2025Article
- Recent Trends in Advanced Glycation End Products in Foods: Formation, Toxicity, and Innovative Strategies for Extraction, Detection, and Inhibition.Foods (Basel, Switzerland) · 2024Review
- Macrophage RAGE activation is proinflammatory in NASH.JCI insight · 2024Article
- Methylglyoxal and Its Adducts: Induction, Repair, and Association with Disease.Chemical research in toxicology · 2022Review
- Heterozygous Loss of KRIT1 in Mice Affects Metabolic Functions of the Liver, Promoting Hepatic Oxidative and Glycative Stress.International journal of molecular sciences · 2022Article
- Targeting Scavenger Receptors in Inflammatory Disorders and Oxidative Stress.Antioxidants (Basel, Switzerland) · 2022Review
- Glycation and a Spark of ALEs (Advanced Lipoxidation End Products) - Igniting RAGE/Diaphanous-1 and Cardiometabolic Disease.Frontiers in cardiovascular medicine · 2022Review
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Advanced glycation endproducts (AGEs) are involved in several diseases, including NAFLD and NASH. RAGE is the main receptor mediating the pro-inflammatory signalling induced by AGEs. Therefore, targeting of RAGE has been proposed for prevention of chronic inflammatory diseases. However, the role of RAGE in the development of NAFLD and NASH remains poorly understood. We thus aimed to analyse the effect of obesity on AGEs accumulation, AGE-receptors and AGE-detoxification, and whether the absence of RAGE might improve hepatosteatosis and inflammation, by comparing the liver of lean control, obese (LeptrDb-/-) and obese RAGE-deficient (RAGE-/- LeptrDb-/-) mice. Obesity induced AGEs accumulation and RAGE expression with hepatosteatosis and inflammation in LeptrDb-/-, compared to lean controls. Despite the genetic deletion of RAGE in the LeptrDb-/- mice, high levels of intrahepatic AGEs were maintained accompanied by decreased expression of the protective AGE-receptor-1, impaired AGE-detoxifying system glyoxalase-1, and increased expression of the alternative AGE-receptor galectin-3. We also found sustained hepatosteatosis and inflammation as determined by persistent activation of the lipogenic SREBP1c and proinflammatory NLRP3 signalling pathways. Thus, RAGE targeting is not effective in the prevention of NAFLD in conditions of obesity, likely due to the direct liver specific crosstalk of RAGE with other AGE-receptors and AGE-detoxifying systems.
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