Year: 2009
Type: article
Abstract: Excess retinoic acid (RA) signaling can be teratogenic and result in cardiac birth defects, but the cellular and molecular origins of these defects are not well understood. Excessive RA signaling can completely eliminate heart formation in the zebrafish embryo. However, atrial and ventricular cells are differentially sensitive to more modest increases in RA signaling. Increased Hox activity, downstream of RA signaling, causes phenotypes similar to those resulting from excess RA. These results suggest that Hox activity mediates the differential effects of ectopic RA on atrial and ventricular cardiomyocytes and may underlie the teratogenic effects of RA on the heart.
Source: Developmental Dynamics
DOI: 10.1002/dvdy.21951
Authors: Joshua S. Waxman, Deborah Yelon
Institutions: NYU Langone Health, New York University
Language: English
Subfield: Molecular Biology
Domain: Life Sciences
Open Access status: bronze
OpenAlex ID: W2030737203
