ArticleBiomolecular concepts2011
ALDOSE REDUCTASE: New Insights for an Old Enzyme.
Article in Biomolecular concepts, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers, 1 of them a synthesis that pooled it.
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
71 citing papers in PubMed, 1 synthesis or guideline pooled it, 180 citations in OpenAlex.
- The Role ofGenes · 2026Pooled it
- Polyphenols in food and food wastes: Extraction, isolation, and health applications.Food chemistry. Molecular sciences · 2026Review
- Hydrazonylthiazole Derivatives as Dual EGFR and ALR2 Inhibitors: Design, Synthesis, and Comprehensive In Vitro and In Silico Evaluation for Potential Anticancer Activity.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Aldose Reductase Inhibition byMolecules (Basel, Switzerland) · 2025Article
- Transcriptomic, biochemical, and microbiome assessments into drought and salinity tolerance in durum wheat mediated by plant growth-promoting bacteria.Physiology and molecular biology of plants : an international journal of functional plant biology · 2025Article
- Role of astrocytes in diabetic neuropathy: Review of their involvement in disease mechanisms.World journal of diabetes · 2025Review
- Naturally derived bioactive compounds as regulators of oxidative stress and inflammation in asthma.Chinese medicine · 2025Review
- Minocycline reduces proinflammatory and oxidative stress markers in the spinal cord and morphology changes in sciatic nerve of Type 2 diabetic neuropathy rat model.Diabetology international · 2025Article
- Oxidative Stress and Cardiovascular Complications in Type 2 Diabetes: From Pathophysiology to Lifestyle Modifications.Antioxidants (Basel, Switzerland) · 2025Review
- Exploration of leads from bis-indole based triazine derivatives targeting human aldose reductase in diabetic type 2: in-silico approaches.3 Biotech · 2025Article
- An Investigation of the Saccharides Profile and Metabolic Gene Expression in Muskrat Scented Glands in Different Secretion Seasons.Animals : an open access journal from MDPI · 2024Article
- Unveiling the Role of Schwann Cell Plasticity in the Pathogenesis of Diabetic Peripheral Neuropathy.International journal of molecular sciences · 2024Review
- SORD-deficient rats develop a motor-predominant peripheral neuropathy unveiling novel pathophysiological insights.Brain : a journal of neurology · 2024Article
- Aldose reductase is a potential therapeutic target for neurodegeneration.Chemico-biological interactions · 2024Review
- AKR1B1 drives hyperglycemia-induced metabolic reprogramming in MASLD-associated hepatocellular carcinoma.JHEP reports : innovation in hepatology · 2024Article
- The Role of Aldose Reductase in Polyol Pathway: An Emerging Pharmacological Target in Diabetic Complications and Associated Morbidities.Current pharmaceutical biotechnology · 2024Review
- AKR1B10 regulates M2 macrophage polarization to promote the malignant phenotype of gastric cancer.Bioscience reports · 2023Article
- Aldehyde Dehydrogenase and Aldo-Keto Reductase Enzymes: Basic Concepts and Emerging Roles in Diabetic Retinopathy.Antioxidants (Basel, Switzerland) · 2023Review
- 6D-QSAR for predicting biological activity of human aldose reductase inhibitors using quasar receptor surface modeling.BMC chemistry · 2023Article
- Sorbitol reduction via govorestat ameliorates synaptic dysfunction and neurodegeneration in sorbitol dehydrogenase deficiency.JCI insight · 2023Article
11 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
In the past years aldose reductase (AKR1B1; AR) is thought to be involved in the pathogenesis of secondary diabetic complications such as retinopathy, neuropathy, nephropathy and cataractogenesis. Subsequently, a number of AR inhibitors have been developed and tested for diabetic complications. Although, these inhibitors have found to be safe for human use, they have not been successful at the clinical studies because of limited efficacy. Recently, the potential physiological role of AR has been reassessed from a different point of view. Diverse groups suggested that AR besides reducing glucose, also efficiently reduces oxidative stress-generated lipid peroxidation-derived aldehydes and their glutathione conjugates. Since lipid aldehydes alter cellular signals by regulating the activation of transcription factors such as NF-kB and AP1, inhibition of AR could inhibit such events. Indeed, a wide array of recent experimental evidence indicates that the inhibition of AR prevents oxidative stress-induced activation of NF-kB and AP1 signals that lead to cell death or growth. Further, AR inhibitors have been shown to prevent inflammatory complications such as sepsis, asthma, colon cancer and uveitis in rodent animal models. The new experimental in-vitro and in-vivo data has provided a basis for investigating the clinical efficacy of AR inhibitors in preventing other inflammatory complications than diabetes. This review describes how the recent studies have identified novel plethoric physiological and pathophysiological significance of AR in mediating inflammatory complications, and how the discovery of such new insights for this old enzyme could have considerable importance in envisioning potential new therapeutic strategies for the prevention or treatment of inflammatory diseases.
Identifiers
What Socratic holds
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 Socratic graph.