ArticleBioMed research international2016
Update on Mechanisms of Renal Tubule Injury Caused by Advanced Glycation End Products.
Article in BioMed research international, 2016. 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, 26 citations in OpenAlex.
- Associations of dietary macronutrients and energy intake with diabetic kidney disease and all-cause mortality in diabetes: evidence from NHANES.BMJ open diabetes research & care · 2026Article
- Advances regarding the mechanism of endoplasmic reticulum stress in diabetic kidney disease and pharmacological interventions (Review).Molecular medicine reports · 2026Review
- Molecular mechanisms attributed to colistin renal proximal tubular epithelial cytotoxicity.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2025Review
- Spinach Extract Reduces Kidney Damage in Diabetic Rats by Impairing the AGEs/RAGE Axis.International journal of molecular sciences · 2025Article
- Autophagy, Pyroptosis and Ferroptosis are Rising Stars in the Pathogenesis of Diabetic Nephropathy.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024Review
- Endoplasmic reticulum stress in diabetic kidney disease: adaptation and apoptosis after three UPR pathways.Apoptosis : an international journal on programmed cell death · 2023Review
- Advances in understanding and treating diabetic kidney disease: focus on tubulointerstitial inflammation mechanisms.Frontiers in endocrinology · 2023Review
- Exploring the mechanisms underlying the therapeutic effect of the drug pair Rhubarb-Coptis in diabetic nephropathy using network pharmacology and molecular docking analysis.Annals of translational medicine · 2022Article
- New insights into the role of empagliflozin on diabetic renal tubular lipid accumulation.Diabetology & metabolic syndrome · 2022Article
- Advanced Glycation End Products and Their Effect on Vascular Complications in Type 2 Diabetes Mellitus.Nutrients · 2022Review
- Advanced Glycation End Products: New Clinical and Molecular Perspectives.International journal of environmental research and public health · 2021Review
- Correlation and Diagnostic Value of Serum RBP4 and sRAGE and the Condition of Patients with Chronic Kidney Disease.Evidence-based complementary and alternative medicine : eCAM · 2021Article
- Dietary Glycotoxins Impair Hepatic Lipidemic Profile in Diet-Induced Obese Rats Causing Hepatic Oxidative Stress and Insulin Resistance.Oxidative medicine and cellular longevity · 2019Article
- Activation of NLRP3 Inflammasome Promotes Foam Cell Formation in Vascular Smooth Muscle Cells and Atherogenesis Via HMGB1.Journal of the American Heart Association · 2018Article
- Role of AGEs in the progression and regression of atherosclerotic plaques.Glycoconjugate journal · 2018Review
- High Glucose Promotes CD36 Expression by Upregulating Peroxisome Proliferator-Activated ReceptorBioMed research international · 2017Article
- ISN Forefronts Symposium 2015: Nuclear Receptors and Diabetic Nephropathy.Kidney international reports · 2016Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetic nephropathy (DN) caused by advanced glycation end products (AGEs) may be associated with lipid accumulation in the kidneys. This study was designed to investigate whether Nε-(carboxymethyl) lysine (CML, a member of the AGEs family) increases lipid accumulation in a human renal tubular epithelial cell line (HK-2) via increasing cholesterol synthesis and uptake and reducing cholesterol efflux through endoplasmic reticulum stress (ERS). Our results showed that CML disrupts cholesterol metabolism in HK-2 cells by activating sterol regulatory element-binding protein 2 (SREBP-2) and liver X receptor (LXR), followed by an increase in 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMG-CoAR) mediated cholesterol synthesis and low density lipoprotein receptor (LDLr) mediated cholesterol uptake and a reduction in ATP-binding cassette transporter A1 (ABCA1) mediated cholesterol efflux, ultimately causing lipid accumulation in HK-2 cells. All of these responses could be suppressed by an ERS inhibitor, which suggests that CML causes lipid accumulation in renal tubule cells through ERS and that the inhibition of ERS is a potential novel approach to treating CML-induced renal tubular foam cell formation.
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