ArticleDiabetes2006
Contribution of aldose reductase to diabetic hyperproliferation of vascular smooth muscle cells.
Article in Diabetes, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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
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Who cites it
33 citing papers in PubMed, 66 citations in OpenAlex.
- Review
- The Role of Aldose Reductase in Polyol Pathway: An Emerging Pharmacological Target in Diabetic Complications and Associated Morbidities.Current pharmaceutical biotechnology · 2024Review
- Physiological and Pathological Roles of Aldose Reductase.Metabolites · 2021Review
- Aldose Reductase: An Emerging Target for Development of Interventions for Diabetic Cardiovascular Complications.Frontiers in endocrinology · 2021Review
- Polymorphisms of Aldose Reductase (ALR2) Regulatory Gene are Risk Factors for Diabetic Retinopathy in Type-2 Diabetes Mellitus Patients in Bali, Indonesia.The open ophthalmology journal · 2018Article
- Article
- Aldose Reductase Inhibitor Protects against Hyperglycemic Stress by Activating Nrf2-Dependent Antioxidant Proteins.Journal of diabetes research · 2017Article
- Delayed reendothelialization with rapamycin is rescued by the addition of nicorandil in balloon-injured rat carotid arteries.Oncotarget · 2016Article
- Nicorandil attenuates carotid intimal hyperplasia after balloon catheter injury in diabetic rats.Cardiovascular diabetology · 2016Article
- 4-Hydroxy-nonenal-A Bioactive Lipid Peroxidation Product.Biomolecules · 2015Review
- Vinpocetine attenuates neointimal hyperplasia in diabetic rat carotid arteries after balloon injury.PloS one · 2014Article
- Implications of autophagy for vascular smooth muscle cell function and plasticity.Free radical biology & medicine · 2013Review
- High glucose induces connective tissue growth factor expression and extracellular matrix accumulation in rat aorta vascular smooth muscle cells via extracellular signal-regulated kinase 1/2.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2013Article
- Oxidized lipids activate autophagy in a JNK-dependent manner by stimulating the endoplasmic reticulum stress response.Redox biology · 2013Article
- Aldose reductase, oxidative stress and diabetic cardiovascular complications.Cardiovascular & hematological agents in medicinal chemistry · 2012Review
- Aldose reductase regulates TNF-α-induced inducible nitric oxide synthase expression in human mesangial cells.Molecular biology reports · 2012Article
- Aldose reductase, oxidative stress, and diabetic mellitus.Frontiers in pharmacology · 2012 · on this mapArticle
- Cellular dysfunction in diabetes as maladaptive response to mitochondrial oxidative stress.Experimental diabetes research · 2012Review
- Cytochromes P450 catalyze the reduction of α,β-unsaturated aldehydes.Chemical research in toxicology · 2011Article
- Aldose reductase (AKR1B3) regulates the accumulation of advanced glycosylation end products (AGEs) and the expression of AGE receptor (RAGE).Chemico-biological interactions · 2011Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The objective of this study was to determine whether the polyol pathway enzyme aldose reductase mediates diabetes abnormalities in vascular smooth muscle cell (SMC) growth. Aldose reductase inhibitors (tolrestat or sorbinil) or antisense aldose reductase mRNA prevented hyperproliferation of cultured rat aortic SMCs induced by high glucose. Cell cycle progression in the presence of high glucose was blocked by tolrestat, which induced a G0-G1 phase growth arrest. In situ, diabetes increased SMC growth and intimal hyperplasia in balloon-injured carotid arteries of streptozotocin-treated rats, when examined 7 or 14 days after injury. Treatment with tolrestat (15 mg x kg(-1) x day(-1)) diminished intimal hyperplasia and decreased SMC content of the lesion by 25%. Although tolrestat treatment increased immunoreactivity of the lesion with antibodies raised against protein adducts of the lipid peroxidation product 4-hydroxy trans-2-nonenal, no compensatory increase in lesion fibrosis was observed. Collectively, these results suggest that inhibition of aldose reductase prevents glucose-induced stimulation of SMC growth in culture and in situ. Even though inhibition of aldose reductase increases vascular oxidative stress, this approach may be useful in preventing abnormal SMC growth in vessels of diabetic patients.
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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 OpenQuestion graph.