Cardiac developmental toxicity

Mahler, Gretchen J.; Butcher, Jonathan T.

doi:10.1002/bdrc.20219

Cited by 22 publications

(17 citation statements)

References 45 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…There have been some data supporting an increased risk of cardiac malformations with an even higher risk if the exposure occurred during the firsttrimester. This includes ventricular outflow defects and atrial/ventricular septal defects 6,7 (Figures 2-4). Fluoxetine (Prozac) and sertraline (Zoloft) are other SSRIs that may be associated with cardiac malformations.…”

Section: Antidepressantsmentioning

confidence: 99%

See 1 more Smart Citation

Teratogens and Congenital Heart Disease

Lynch

Abel

2015

Journal of Diagnostic Medical Sonography

View full text Add to dashboard Cite

The antenatal diagnosis of fetal congenital heart disease (CHD) allows for identification of potentially life-threatening conditions that may occur in the early neonatal period. A suspicion of congenital heart disease often occurs during the routine fetal anatomical survey. Subsequently, fetal echocardiography allows for a more detailed assessment of the cardiac lesion that is necessary in order to plan for delivery and postnatal surgical management. To enhance detection of congenital cardiac anomalies, and in particular ones that are potentially serious, it is important for the obstetrical sonographer to have an understanding of potential teratogenic agents associated with an increased risk of congenital heart disease.

show abstract

Section: Antidepressantsmentioning

confidence: 99%

“…In small studies, it was found to be associated with left outflow tract defects. 7 Importantly, data for all antidepressants are conflicting. There has not been a single antidepressant that has been definitively associated with CHD.…”

Section: Antidepressantsmentioning

confidence: 99%

Teratogens and Congenital Heart Disease

Lynch

Abel

2015

Journal of Diagnostic Medical Sonography

View full text Add to dashboard Cite

show abstract

“…Congenital heart defects arise when genetic and/or environmental perturbations undermine normal cardiac development (reviewed by Bruneau, 2008;Epstein, 2010;Mahler and Butcher, 2011;Srivastava and Olson, 2000). As a class, they cause significant mortality during all stages of human life (Roger et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

Zebrafish second heart field development relies on progenitor specification in anterior lateral plate mesoderm and nkx2.5 function

et al. 2013

View full text Add to dashboard Cite

SUMMARYSecond heart field (SHF) progenitors perform essential functions during mammalian cardiogenesis. We recently identified a population of cardiac progenitor cells (CPCs) in zebrafish expressing latent TGFβ-binding protein 3 (ltbp3) that exhibits several defining characteristics of the anterior SHF in mammals. However, ltbp3 transcripts are conspicuously absent in anterior lateral plate mesoderm (ALPM), where SHF progenitors are specified in higher vertebrates. Instead, ltbp3 expression initiates at the arterial pole of the developing heart tube. Because the mechanisms of cardiac development are conserved evolutionarily, we hypothesized that zebrafish SHF specification also occurs in the ALPM. To test this hypothesis, we Cre/loxP lineage traced gata4 + and nkx2.5 + ALPM populations predicted to contain SHF progenitors, based on evolutionary conservation of ALPM patterning. Traced cells were identified in SHFderived distal ventricular myocardium and in three lineages in the outflow tract (OFT). We confirmed the extent of contributions made by ALPM nkx2.5 + cells using Kaede photoconversion. Taken together, these data demonstrate that, as in higher vertebrates, zebrafish SHF progenitors are specified within the ALPM and express nkx2.5. Furthermore, we tested the hypothesis that Nkx2.5 plays a conserved and essential role during zebrafish SHF development. Embryos injected with an nkx2.5 morpholino exhibited SHF phenotypes caused by compromised progenitor cell proliferation. Co-injecting low doses of nkx2.5 and ltbp3 morpholinos revealed a genetic interaction between these factors. Taken together, our data highlight two conserved features of zebrafish SHF development, reveal a novel genetic relationship between nkx2.5 and ltbp3, and underscore the utility of this model organism for deciphering SHF biology.KEY WORDS: Gata4, Heart development, Lineage tracing, Nkx2.5, Second heart field, ZebrafishZebrafish second heart field development relies on progenitor specification in anterior lateral plate mesoderm and nkx2.5 function

show abstract

“…All things considered, however, at this time it appears safe to say that the minimum of 80% given by van Mil et al (2010) is useful as a guideline for estimating the role of gene-environment interactions as the cause of CHD. The extraordinary complexity of gene-gene and gene-environment interactions in development is just beginning to be appreciated in the early 21 st century (Finnell et al, 2004(Finnell et al, , 2008Zhu et al, 2009;van Mil et al, 2010;Hobbs et al, 2011;Mahler and Butcher, 2011).…”

Section: Introductionmentioning

confidence: 99%

Folate, Homocysteine and the Cardiac Neural Crest

Rosenquist

2013

Developmental Dynamics

View full text Add to dashboard Cite

Congenital heart defects (CHD) are the most common congenital defects worldwide, and perigestational folate supplementation (PFS) is the most effective large-scale intervention to date for reducing CHD. This review is based upon the following premises: that the majority of CHD result from disruption of development of the cardiac neural crest (CNC); and that the CNC is highly responsive to folate and homocysteine. The following roles of folate are discussed in relation to CNC development: one-carbon metabolism in support of mitosis and gene methylation; and gene regulation via direct activity of the folate receptor. The following roles of hyperhomocysteinemia are discussed in the same context: increased oxidative stress; disruption of gene methylation; homocysteinylation of key proteins; and NMDA receptor binding. It is proposed that well-focused advances in folate-CNC research could lead to development of strategies, in addition to PFS, to facilitate normal CNC and heart development, and thereby further reduce CHD.

show abstract

Cardiac developmental toxicity

Cited by 22 publications

References 45 publications

Teratogens and Congenital Heart Disease

Teratogens and Congenital Heart Disease

Zebrafish second heart field development relies on progenitor specification in anterior lateral plate mesoderm and nkx2.5 function

Folate, Homocysteine and the Cardiac Neural Crest

Contact Info

Product

Resources

About