ArticleEndocrinology2010
Aldose reductase regulates vascular smooth muscle cell proliferation by modulating G1/S phase transition of cell cycle.
Article in Endocrinology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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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.
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Who cites it
19 citing papers in PubMed, 35 citations in OpenAlex.
- Review
- Cucurbitacins mitigate vascular neointimal hyperplasia by suppressing cyclin A2 expression and inhibiting VSMC proliferation.Animal models and experimental medicine · 2024Article
- The Role of Aldose Reductase in Polyol Pathway: An Emerging Pharmacological Target in Diabetic Complications and Associated Morbidities.Current pharmaceutical biotechnology · 2024Review
- Roles, molecular mechanisms, and signaling pathways of TMEMs in neurological diseases.American journal of translational research · 2021Review
- MiR-573 suppresses cell proliferation, migration and invasion via regulation of E2F3 in pancreatic cancer.Journal of Cancer · 2021Article
- Aldose Reductase: An Emerging Target for Development of Interventions for Diabetic Cardiovascular Complications.Frontiers in endocrinology · 2021Review
- Stereoselectivity of Aldose Reductase in the Reduction of Glutathionyl-Hydroxynonanal Adduct.Antioxidants (Basel, Switzerland) · 2019Article
- MicroRNA-34a suppresses aggressiveness of hepatocellular carcinoma by modulatingCancer management and research · 2019Article
- Investigation of synergistic mechanism and identification of interaction site of aldose reductase with the combination of gigantol and syringic acid for prevention of diabetic cataract.BMC complementary and alternative medicine · 2016Article
- E2F-1 overexpression inhibits human gastric cancer MGC-803 cell growth in vivo.World journal of gastroenterology · 2015Article
- Nestin downregulation in rat vascular smooth muscle cells represents an early marker of vascular disease in experimental type I diabetes.Cardiovascular diabetology · 2014Article
- Lipid peroxidation: production, metabolism, and signaling mechanisms of malondialdehyde and 4-hydroxy-2-nonenal.Oxidative medicine and cellular longevity · 2014Review
- 4-Hydroxynonenal in the pathogenesis and progression of human diseases.Current medicinal chemistry · 2014Review
- Aldose reductase from Schistosoma japonicum: crystallization and structure-based inhibitor screening for discovering antischistosomal lead compounds.Parasites & vectors · 2013Article
- Molecular cloning and characterization of Schistosoma japonicum aldose reductase.Parasitology research · 2013Article
- Inhibition of vascular smooth muscle cell proliferation by Gentiana lutea root extracts.PloS one · 2013Article
- Article
- Silencing of sodium-hydrogen exchanger 1 attenuates the proliferation, hypertrophy, and migration of pulmonary artery smooth muscle cells via E2F1.American journal of respiratory cell and molecular biology · 2011Article
- ALDOSE REDUCTASE: New Insights for an Old Enzyme.Biomolecular concepts · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Abnormal proliferation of vascular smooth muscle cells (VSMC) is a key feature of development of cardiovascular complications, atherosclerosis, and restenosis. Patients with diabetes have higher risk for restenosis after coronary angioplasty than nondiabetic patients due to hyperglycemia-induced release of cytokines such as TNF-alpha. However, the molecular mechanisms regulating VSMC proliferation remain unclear. Herein, we report that inhibition of the polyol pathway enzyme aldose reductase (AR) prevents high glucose (HG)- and/or TNF-alpha-induced VSMC proliferation by accumulating cells at the G1 phase of the cell cycle. Treatment of VSMC with AR inhibitor sorbinil prevented HG- as well as TNF-alpha-induced phosphorylation of retinoblastoma protein and activation of E2F-1. Inhibition of AR also prevented HG- and TNF-alpha-induced phosphorylation of cyclin-dependent kinase (cdk)-2 and expression of G1/S transition regulatory proteins such as cyclin D1, cyclin E, cdk-4, c-myc, and proliferative cell nuclear antigen. More importantly, inhibition of AR prevented the increased expression of E2F-1 and proliferative cell nuclear antigen in diabetic rat aorta. Treatment of VSMC with the most abundant and toxic lipid aldehyde 4-hydroxy-trans-2-nonenal (HNE) or its glutathione conjugate [glutathionyl (GS)-HNE] or AR-catalyzed product of GS-HNE, GS-1,4-dihydroxynonane, resulted in increased E2F-1 expression. Inhibition of AR prevented HNE- or GS-HNE-induced but not GS-1,4-dihydroxynonane-induced up-regulation of E2F-1. Collectively, these results show that AR could regulate HG- and TNF-alpha-induced VSMC proliferation by altering the activation of G1/S-phase proteins such as E2F-1, cdks, and cyclins. Thus, inhibition of AR may be a useful therapeutic approach in preventing vascular complications.
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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.