ArticleChemico-biological interactions2011
Aldose reductase (AKR1B3) regulates the accumulation of advanced glycosylation end products (AGEs) and the expression of AGE receptor (RAGE).
Article in Chemico-biological interactions, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 31 citations in OpenAlex.
- Reactive carbonyl species in health and chronic disease: from methylglyoxal to an integrative network of metabolic regulation.Cardiovascular diabetology · 2026Review
- Anti-Glycation and Anti-Aging Efficacy of Newly Synthesized Antioxidant With Autophagy Stimulating Activity.Journal of cosmetic dermatology · 2025Article
- Metabolic pathways for removing reactive aldehydes are diminished in the skeletal muscle during heart failure.Skeletal muscle · 2024Article
- Metabolic Pathways for Removing Reactive Aldehydes are Diminished in Atrophic Muscle During Heart Failure.Research square · 2023Article
- The Potential of Dietary Bioactive Compounds against SARS-CoV-2 and COVID-19-Induced Endothelial Dysfunction.Molecules (Basel, Switzerland) · 2022Review
- Deletion of RAGE fails to prevent hepatosteatosis in obese mice due to impairment of other AGEs receptors and detoxifying systems.Scientific reports · 2021Article
- Aldose Reductase: a cause and a potential target for the treatment of diabetic complications.Archives of pharmacal research · 2021Review
- Complement Properdin Regulates the Metabolo-Inflammatory Response to a High Fat Diet.Medicina (Kaunas, Lithuania) · 2020Article
- Effect of rutin on retinal VEGF, TNF-α, aldose reductase, and total antioxidant capacity in diabetic rats: molecular mechanism and ocular pharmacokinetics.International ophthalmology · 2020Article
- Exercise alters and β-alanine combined with exercise augments histidyl dipeptide levels and scavenges lipid peroxidation products in human skeletal muscle.Journal of applied physiology (Bethesda, Md. : 1985) · 2018Article
- Deficiency of aldose reductase exacerbates early pressure overload-induced cardiac dysfunction and autophagy in mice.Journal of molecular and cellular cardiology · 2018Article
- Aldose reductase (AKR1B) deficiency promotes phagocytosis in bone marrow derived mouse macrophages.Chemico-biological interactions · 2017Article
- Mitochondrial dysfunction and tissue injury by alcohol, high fat, nonalcoholic substances and pathological conditions through post-translational protein modifications.Redox biology · 2014Review
- Methylglyoxal, obesity, and diabetes.Endocrine · 2013Review
- Cardiovascular redox and ox stress proteomics.Antioxidants & redox signaling · 2012Review
- Depressed levels of prostaglandin F2α in mice lacking Akr1b7 increase basal adiposity and predispose to diet-induced obesity.Diabetes · 2012Article
- Urinary levels of the acrolein conjugates of carnosine are associated with inhaled toxicants.Inhalation toxicologyArticle
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4 authors at 1 institution in 1 country.
Funding
Abstract
Diabetes results in enhanced chemical modification of proteins by advanced lipoxidation end products (ALEs) and advanced glycation end products (AGEs) precursors. These modifications have been linked to the development of several secondary diabetic complications. Our previous studies showed that aldose reductase (AR; AKR1B3) catalyzes the reduction of ALEs and AGEs precursors; however, the in vivo significance of this metabolic pathway during diabetes and obesity has not been fully assessed. Therefore we examined the role of AR in regulating ALEs and AGEs formation in murine models of diet-induced obesity and streptozotocin-induced diabetes. In comparison with wild-type (WT) and AR-null mice fed normal chow, mice fed a high-fat (HF) diet (42% kcal fat) showed increased accumulation of AGEs and protein-acrolein adducts in the plasma. AGEs and acrolein adducts were also increased in the epididymal fat of WT and AR-null mice fed a HF diet. Deletion of AR increased the accumulation of 4-hydroxy-trans-2-nonenal (HNE) protein adduct in the plasma and increased the expression of the AGE receptor (RAGE) in HF fed mice. No change in AGEs formation was observed in the kidneys of HF-fed mice. In comparison, renal tissue from AR-null mice treated with streptozotocin showed greater AGE accumulation than streptozotocin-treated WT mice. These data indicated that AR regulated the accumulation of lipid peroxidation derived aldehydes and AGEs under conditions of severe, but not mild, hyperglycemia and that deletion of AR increased RAGE-induction via mechanisms that were independent of AGEs accumulation.
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