Abstract
Substantial experimental and epidemiological data have highlighted the interplay between nutritional and genetic factors in the development of congenital heart defects. Retinoic acid (RA), a derivative of vitamin A, plays a key role during vertebrate development including the formation of the heart. Retinoids bind to RA and retinoid X receptors (RARs and RXRs) which then regulate tissue-specific genes. Here, we will focus on the roles of RA signaling and receptors in gene regulation during cardiogenesis, and the consequence of deregulated retinoid signaling on heart formation and congenital heart defects.
Keywords:
Cell fate decisions; Heart development; Retinoic acid; Retinoic acid receptors.
Copyright © 2016 Elsevier Ireland Ltd. All rights reserved.
Publication types
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Review
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Research Support, Non-U.S. Gov't
MeSH terms
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Aldehyde Oxidoreductases / genetics
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Aldehyde Oxidoreductases / metabolism
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Animals
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Drosophila melanogaster / embryology
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Drosophila melanogaster / genetics
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Drosophila melanogaster / metabolism
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Gene Expression Regulation, Developmental*
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Heart / embryology*
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Homeodomain Proteins / genetics
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Homeodomain Proteins / metabolism
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Humans
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LIM-Homeodomain Proteins / genetics
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LIM-Homeodomain Proteins / metabolism
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Mice
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Organogenesis / genetics*
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Retinoid X Receptors / genetics*
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Retinoid X Receptors / metabolism
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Signal Transduction
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Transcription Factors / genetics
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Transcription Factors / metabolism
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Tretinoin / metabolism*
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Zebrafish / embryology
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Zebrafish / genetics
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Zebrafish / metabolism
Substances
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Homeodomain Proteins
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LIM-Homeodomain Proteins
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Retinoid X Receptors
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Transcription Factors
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insulin gene enhancer binding protein Isl-1
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Tretinoin
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Aldehyde Oxidoreductases
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RALDH2 protein, mouse