Hyperglycemia-Induced Aberrant Cell Proliferation; A Metabolic Challenge Mediated by Protein O-GlcNAc Modification

Chronic hyperglycemia has been associated with an increased prevalence of pathological conditions including cardiovascular disease, cancer, or various disorders of the immune system. In some cases, these associations may be traced back to a common underlying cause, but more often, hyperglycemia and...

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Main Authors: Tamás Nagy, Viktória Fisi, Dorottya Frank, Emese Kátai, Zsófia Nagy, Attila Miseta
Format: Article
Language:English
Published: MDPI AG 2019-08-01
Series:Cells
Subjects:
Online Access:https://www.mdpi.com/2073-4409/8/9/999
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author Tamás Nagy
Viktória Fisi
Dorottya Frank
Emese Kátai
Zsófia Nagy
Attila Miseta
author_facet Tamás Nagy
Viktória Fisi
Dorottya Frank
Emese Kátai
Zsófia Nagy
Attila Miseta
author_sort Tamás Nagy
collection DOAJ
description Chronic hyperglycemia has been associated with an increased prevalence of pathological conditions including cardiovascular disease, cancer, or various disorders of the immune system. In some cases, these associations may be traced back to a common underlying cause, but more often, hyperglycemia and the disturbance in metabolic balance directly facilitate pathological changes in the regular cellular functions. One such cellular function crucial for every living organism is cell cycle regulation/mitotic activity. Although metabolic challenges have long been recognized to influence cell proliferation, the direct impact of diabetes on cell cycle regulatory elements is a relatively uncharted territory. Among other “nutrient sensing” mechanisms, protein O-linked β-N-acetylglucosamine (O-GlcNAc) modification emerged in recent years as a major contributor to the deleterious effects of hyperglycemia. An increasing amount of evidence suggest that O-GlcNAc may significantly influence the cell cycle and cellular proliferation. In our present review, we summarize the current data available on the direct impact of metabolic changes caused by hyperglycemia in pathological conditions associated with cell cycle disorders. We also review published experimental evidence supporting the hypothesis that O-GlcNAc modification may be one of the missing links between metabolic regulation and cellular proliferation.
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spelling doaj.art-9ab15caa3c8e4722bf0704ed1f5b6ab42023-09-02T17:18:18ZengMDPI AGCells2073-44092019-08-018999910.3390/cells8090999cells8090999Hyperglycemia-Induced Aberrant Cell Proliferation; A Metabolic Challenge Mediated by Protein O-GlcNAc ModificationTamás Nagy0Viktória Fisi1Dorottya Frank2Emese Kátai3Zsófia Nagy4Attila Miseta5Department of Laboratory Medicine, Medical School, University of Pécs, H-7624 Pécs, HungaryDepartment of Laboratory Medicine, Medical School, University of Pécs, H-7624 Pécs, HungaryDepartment of Dentistry, Oral and Maxillofacial Surgery, Medical School, University of Pécs, H-7621 Pécs, HungaryDepartment of Laboratory Medicine, Medical School, University of Pécs, H-7624 Pécs, HungaryDepartment of Laboratory Medicine, Medical School, University of Pécs, H-7624 Pécs, HungaryDepartment of Laboratory Medicine, Medical School, University of Pécs, H-7624 Pécs, HungaryChronic hyperglycemia has been associated with an increased prevalence of pathological conditions including cardiovascular disease, cancer, or various disorders of the immune system. In some cases, these associations may be traced back to a common underlying cause, but more often, hyperglycemia and the disturbance in metabolic balance directly facilitate pathological changes in the regular cellular functions. One such cellular function crucial for every living organism is cell cycle regulation/mitotic activity. Although metabolic challenges have long been recognized to influence cell proliferation, the direct impact of diabetes on cell cycle regulatory elements is a relatively uncharted territory. Among other “nutrient sensing” mechanisms, protein O-linked β-N-acetylglucosamine (O-GlcNAc) modification emerged in recent years as a major contributor to the deleterious effects of hyperglycemia. An increasing amount of evidence suggest that O-GlcNAc may significantly influence the cell cycle and cellular proliferation. In our present review, we summarize the current data available on the direct impact of metabolic changes caused by hyperglycemia in pathological conditions associated with cell cycle disorders. We also review published experimental evidence supporting the hypothesis that O-GlcNAc modification may be one of the missing links between metabolic regulation and cellular proliferation.https://www.mdpi.com/2073-4409/8/9/999diabetesO-GlcNAcproliferationcell cyclecancerhyperglycemia
spellingShingle Tamás Nagy
Viktória Fisi
Dorottya Frank
Emese Kátai
Zsófia Nagy
Attila Miseta
Hyperglycemia-Induced Aberrant Cell Proliferation; A Metabolic Challenge Mediated by Protein O-GlcNAc Modification
Cells
diabetes
O-GlcNAc
proliferation
cell cycle
cancer
hyperglycemia
title Hyperglycemia-Induced Aberrant Cell Proliferation; A Metabolic Challenge Mediated by Protein O-GlcNAc Modification
title_full Hyperglycemia-Induced Aberrant Cell Proliferation; A Metabolic Challenge Mediated by Protein O-GlcNAc Modification
title_fullStr Hyperglycemia-Induced Aberrant Cell Proliferation; A Metabolic Challenge Mediated by Protein O-GlcNAc Modification
title_full_unstemmed Hyperglycemia-Induced Aberrant Cell Proliferation; A Metabolic Challenge Mediated by Protein O-GlcNAc Modification
title_short Hyperglycemia-Induced Aberrant Cell Proliferation; A Metabolic Challenge Mediated by Protein O-GlcNAc Modification
title_sort hyperglycemia induced aberrant cell proliferation a metabolic challenge mediated by protein o glcnac modification
topic diabetes
O-GlcNAc
proliferation
cell cycle
cancer
hyperglycemia
url https://www.mdpi.com/2073-4409/8/9/999
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AT attilamiseta hyperglycemiainducedaberrantcellproliferationametabolicchallengemediatedbyproteinoglcnacmodification