TNFalpha in the Pathogenesis of Diabetes-Induced Embryopathies: Functions and Targets

Hyperglycemia-induced increase in the production of reactive oxygen species (ROS) is proposed to be an initial step in the pathogenesis of diabetes-induced spontaneous abortions and structural inborn anomalies. However, the subsequent steps in this process are incompletely understood. One of the key...

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Main Authors: Torchinsky, Arkady, Toder, Vladimir
Formato: Artigo
Idioma:English
Publicado em: SBDR - Society for Biomedical Diabetes Research 2007
Assuntos:
Editorial
Acesso em linha:https://ncbi.nlm.nih.gov/pmc/articles/PMC2270405/
https://ncbi.nlm.nih.gov/pubmed/18338073
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1900/RDS.2007.4.200
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spelling pubmed-22704052009-02-10 TNFalpha in the Pathogenesis of Diabetes-Induced Embryopathies: Functions and Targets Torchinsky, Arkady Toder, Vladimir Rev Diabet Stud Editorial Hyperglycemia-induced increase in the production of reactive oxygen species (ROS) is proposed to be an initial step in the pathogenesis of diabetes-induced spontaneous abortions and structural inborn anomalies. However, the subsequent steps in this process are incompletely understood. One of the key molecules involved is tumor necrosis factor-alpha (TNFα): its expression is regulated by ROS and it regulates ROS production in turn. This cytokine has been the focus of many studies addressing the mechanisms of different forms of diabetes-induced embryopathies, such as early pregnancy loss, inborn anomalies, fetal growth retardation as well as some pathologies appearing during adult life. In this review, we analyze the results of these studies and discuss how TNFα may regulate the response of pre- and post-implantation stage embryos to diabetes-induced detrimental stimuli. The data presented in this review suggest that TNFα may play a dual role in the pathogenesis of diabetes-induced embryopathies. It may act both as a mediator of diabetes-induced embryotoxic stimuli leading to the death of peri-implantation stage embryos and, possibly, as a suppressor of diabetes-induced apoptosis in post-implantation stage embryos. It also appears that TNFα fulfills these functions via interaction with leukemia inhibitory factor (LIF) and the transcription factor NF-κB. These molecules are presently considered as attractive targets for the treatment of diabetes-induced complications. Therefore, further studies addressing their role in the mechanisms underlying diabetes-induced embryopathies are needed to evaluate the safety of such therapies for diabetic women of childbearing age. SBDR - Society for Biomedical Diabetes Research 2007 2008-02-10 /pmc/articles/PMC2270405/ /pubmed/18338073 http://dx.doi.org/10.1900/RDS.2007.4.200 Text en Copyright © 2007, SBDR - Society for Biomedical Diabetes Research
institution US National Library of Medicine
collection PubMed Central
language English
format Article
topic Editorial
spellingShingle Editorial
Torchinsky, Arkady
Toder, Vladimir
TNFalpha in the Pathogenesis of Diabetes-Induced Embryopathies: Functions and Targets
description Hyperglycemia-induced increase in the production of reactive oxygen species (ROS) is proposed to be an initial step in the pathogenesis of diabetes-induced spontaneous abortions and structural inborn anomalies. However, the subsequent steps in this process are incompletely understood. One of the key molecules involved is tumor necrosis factor-alpha (TNFα): its expression is regulated by ROS and it regulates ROS production in turn. This cytokine has been the focus of many studies addressing the mechanisms of different forms of diabetes-induced embryopathies, such as early pregnancy loss, inborn anomalies, fetal growth retardation as well as some pathologies appearing during adult life. In this review, we analyze the results of these studies and discuss how TNFα may regulate the response of pre- and post-implantation stage embryos to diabetes-induced detrimental stimuli. The data presented in this review suggest that TNFα may play a dual role in the pathogenesis of diabetes-induced embryopathies. It may act both as a mediator of diabetes-induced embryotoxic stimuli leading to the death of peri-implantation stage embryos and, possibly, as a suppressor of diabetes-induced apoptosis in post-implantation stage embryos. It also appears that TNFα fulfills these functions via interaction with leukemia inhibitory factor (LIF) and the transcription factor NF-κB. These molecules are presently considered as attractive targets for the treatment of diabetes-induced complications. Therefore, further studies addressing their role in the mechanisms underlying diabetes-induced embryopathies are needed to evaluate the safety of such therapies for diabetic women of childbearing age.
author Torchinsky, Arkady
Toder, Vladimir
author_facet Torchinsky, Arkady
Toder, Vladimir
author_sort Torchinsky, Arkady
title TNFalpha in the Pathogenesis of Diabetes-Induced Embryopathies: Functions and Targets
title_short TNFalpha in the Pathogenesis of Diabetes-Induced Embryopathies: Functions and Targets
title_full TNFalpha in the Pathogenesis of Diabetes-Induced Embryopathies: Functions and Targets
title_fullStr TNFalpha in the Pathogenesis of Diabetes-Induced Embryopathies: Functions and Targets
title_full_unstemmed TNFalpha in the Pathogenesis of Diabetes-Induced Embryopathies: Functions and Targets
title_sort tnfalpha in the pathogenesis of diabetes-induced embryopathies: functions and targets
publisher SBDR - Society for Biomedical Diabetes Research
publisher_facet SBDR - Society for Biomedical Diabetes Research
publishDate 2007
url https://ncbi.nlm.nih.gov/pmc/articles/PMC2270405/
https://ncbi.nlm.nih.gov/pubmed/18338073
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1900/RDS.2007.4.200
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