ArticleCell stress & chaperones2014
AKR1B10 is induced by hyperglycaemia and lipopolysaccharide in patients with diabetic nephropathy.
Article in Cell stress & chaperones, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 27 citations in OpenAlex.
- Elucidating the therapeutic targets and multi-target mechanisms of salvianolic acid A for diabetic nephropathy.Mammalian genome : official journal of the International Mammalian Genome Society · 2026Article
- Aldo-keto reductase family 1 member B10 prevents esophageal squamous cell carcinoma from reactive carbonyl species-induced cell death and promotes its progression.Cancer cell international · 2024Article
- Review
- AKR1B10 and digestive tumors development: a review.Frontiers in immunology · 2024Review
- AKR1B10 regulates M2 macrophage polarization to promote the malignant phenotype of gastric cancer.Bioscience reports · 2023Article
- Relationship Between Hepatic Gene Expression, Intestinal Microbiota, and Inferred Functional Metagenomic Analysis in NAFLD.Clinical and translational gastroenterology · 2022Article
- AKR1B10, One of the Triggers of Cytokine Storm in SARS-CoV2 Severe Acute Respiratory Syndrome.International journal of molecular sciences · 2022Article
- AKR1B10 as a Potential Novel Serum Biomarker for Breast Cancer: A Pilot Study.Frontiers in oncology · 2022Article
- Three dimensional modeling of biologically relevant fluid shear stress in human renal tubule cells mimics in vivo transcriptional profiles.Scientific reports · 2021Article
- The Role of AKR1B10 in Physiology and Pathophysiology.Metabolites · 2021Review
- Uncovering genetic mechanisms of hypertension through multi-omic analysis of the kidney.Nature genetics · 2021Article
- Exploring the Molecular Mechanism of Liuwei Dihuang Pills for Treating Diabetic Nephropathy by Combined Network Pharmacology and Molecular Docking.Evidence-based complementary and alternative medicine : eCAM · 2021Article
- Article
- AKR1B1 Upregulation Contributes to Neuroinflammation and Astrocytes Proliferation by Regulating the Energy Metabolism in Rat Spinal Cord Injury.Neurochemical research · 2018Review
- Potential of AKR1B10 as a Biomarker and Therapeutic Target in Type 2 Leprosy Reaction.Frontiers in medicine · 2018Article
- Transcriptomic alterations in the heart of non-obese type 2 diabetic Goto-Kakizaki rats.Cardiovascular diabetology · 2016Article
- Copy-number variation associated with congenital anomalies of the kidney and urinary tract.Pediatric nephrology (Berlin, Germany) · 2015Article
- Expression of aldo-keto reductase family 1 member b10 in the early stages of human hepatocarcinogenesis.International journal of molecular sciences · 2014Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aldose reductase family member B10 (AKR1B10) belongs to the aldo-keto reductase gene superfamily and is closely related to aldose reductase (AKR1B1). It has been shown that AKR1B10 is present in many of the same human tissues as AKR1B1. The objective of this study was to investigate whether AKR1B10 has a role in diabetic nephropathy (DN) by investigating its response to high glucose and inflammation, both of which have been associated with the development and progression of DN. Expression levels of AKR1B10 were determined in peripheral blood mononuclear cells (PBMCs) obtained from 25 patients with type 1 diabetes and nephropathy, 25 without DN and 25 normal healthy controls that were exposed to high glucose (25 mM D-glucose) and also the inflammatory stressor lipopolysaccharide (LPS, 10 μm). Under high glucose and LPS conditions, there was a significant increase in the expression of AKR1B10 in the PBMCs from patients with DN compared to those without DN and the normal controls. In conclusion, these results suggest that AKR1B10 may have an important role in the development and progression of DN.
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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.