Nuclear factor of activated T-cells transcription factors in the vasculature: the good guys or the bad guys?

The nuclear factor of activated T-cells (NFAT) proteins are a family of Ca/calcineurin-dependent transcription factors that were first characterized in T-lymphocytes as inducers of cytokine gene expression. Since then, NFAT proteins have been shown to play varied roles outside of the immune system,...

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Published inCurrent opinion in lipidology Vol. 19; no. 5; p. 483
Main Authors Nilsson, Lisa M, Nilsson-Ohman, Jenny, Zetterqvist, Anna V, Gomez, Maria F
Format Journal Article
LanguageEnglish
Published England 01.10.2008
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Abstract The nuclear factor of activated T-cells (NFAT) proteins are a family of Ca/calcineurin-dependent transcription factors that were first characterized in T-lymphocytes as inducers of cytokine gene expression. Since then, NFAT proteins have been shown to play varied roles outside of the immune system, including in the cardiovascular system. Cells in the vessel wall display a diverse array of Ca signaling modalities, which are subject to change during disease. The fact that NFAT proteins are able to decode and translate these signals into changes in gene expression makes them potential regulators of vascular pathogenesis. It is now clear that NFAT signaling is required for normal vascular patterning during embryogenesis and for vascular endothelial growth factor-induced angiogenesis. The overall role of NFAT signaling in the vasculature, however, is less clear during adult life. This review aims to give an update on mechanisms that regulate NFAT activation in vascular cells, with an emphasis on the role of mitochondria and of upstream activators such as lipids and glucose. It also addresses recent work implicating NFAT proteins as mediators of vascular disease. A better understanding of the NFAT-signaling pathway in the vasculature may open up an unexplored area for the development of new therapeutic approaches for treating vascular disease.
AbstractList The nuclear factor of activated T-cells (NFAT) proteins are a family of Ca/calcineurin-dependent transcription factors that were first characterized in T-lymphocytes as inducers of cytokine gene expression. Since then, NFAT proteins have been shown to play varied roles outside of the immune system, including in the cardiovascular system. Cells in the vessel wall display a diverse array of Ca signaling modalities, which are subject to change during disease. The fact that NFAT proteins are able to decode and translate these signals into changes in gene expression makes them potential regulators of vascular pathogenesis. It is now clear that NFAT signaling is required for normal vascular patterning during embryogenesis and for vascular endothelial growth factor-induced angiogenesis. The overall role of NFAT signaling in the vasculature, however, is less clear during adult life. This review aims to give an update on mechanisms that regulate NFAT activation in vascular cells, with an emphasis on the role of mitochondria and of upstream activators such as lipids and glucose. It also addresses recent work implicating NFAT proteins as mediators of vascular disease. A better understanding of the NFAT-signaling pathway in the vasculature may open up an unexplored area for the development of new therapeutic approaches for treating vascular disease.
Author Zetterqvist, Anna V
Gomez, Maria F
Nilsson, Lisa M
Nilsson-Ohman, Jenny
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  fullname: Gomez, Maria F
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Snippet The nuclear factor of activated T-cells (NFAT) proteins are a family of Ca/calcineurin-dependent transcription factors that were first characterized in...
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StartPage 483
SubjectTerms Animals
Blood Vessels - cytology
Blood Vessels - metabolism
Blood Vessels - physiology
Calcium - metabolism
Glucose - metabolism
Humans
Lipid Metabolism
Mitochondria - metabolism
Models, Biological
NFATC Transcription Factors - metabolism
NFATC Transcription Factors - physiology
Signal Transduction - physiology
Title Nuclear factor of activated T-cells transcription factors in the vasculature: the good guys or the bad guys?
URI https://www.ncbi.nlm.nih.gov/pubmed/18769229
Volume 19
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