Multiple Roles of Pitx2 in Cardiac Development and Disease
Identifikátory výsledku
Kód výsledku v IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11110%2F17%3A10373132" target="_blank" >RIV/00216208:11110/17:10373132 - isvavai.cz</a>
Nalezeny alternativní kódy
RIV/67985823:_____/17:00506622
Výsledek na webu
<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5753117/" target="_blank" >https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5753117/</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.3390/jcdd4040016" target="_blank" >10.3390/jcdd4040016</a>
Alternativní jazyky
Jazyk výsledku
angličtina
Název v původním jazyce
Multiple Roles of Pitx2 in Cardiac Development and Disease
Popis výsledku v původním jazyce
Cardiac development is a complex morphogenetic process initiated as bilateral cardiogenic mesoderm is specified at both sides of the gastrulating embryo. Soon thereafter, these cardiogenic cells fuse at the embryonic midline configuring a symmetrical linear cardiac tube. Left/right bilateral asymmetry is first detected in the forming heart as the cardiac tube bends to the right, and subsequently, atrial and ventricular chambers develop. Molecular signals emanating from the node confer distinct left/right signalling pathways that ultimately lead to activation of the homeobox transcription factor Pitx2 in the left side of distinct embryonic organ anlagen, including the developing heart. Asymmetric expression of Pitx2 has therefore been reported during different cardiac developmental stages, and genetic deletion of Pitx2 provided evidence of key regulatory roles of this transcription factor during cardiogenesis and thus congenital heart diseases. More recently, impaired Pitx2 function has also been linked to arrhythmogenic processes, providing novel roles in the adult heart. In this manuscript, we provide a state-of-the-art review of the fundamental roles of Pitx2 during cardiogenesis, arrhythmogenesis and its contribution to congenital heart diseases.
Název v anglickém jazyce
Multiple Roles of Pitx2 in Cardiac Development and Disease
Popis výsledku anglicky
Cardiac development is a complex morphogenetic process initiated as bilateral cardiogenic mesoderm is specified at both sides of the gastrulating embryo. Soon thereafter, these cardiogenic cells fuse at the embryonic midline configuring a symmetrical linear cardiac tube. Left/right bilateral asymmetry is first detected in the forming heart as the cardiac tube bends to the right, and subsequently, atrial and ventricular chambers develop. Molecular signals emanating from the node confer distinct left/right signalling pathways that ultimately lead to activation of the homeobox transcription factor Pitx2 in the left side of distinct embryonic organ anlagen, including the developing heart. Asymmetric expression of Pitx2 has therefore been reported during different cardiac developmental stages, and genetic deletion of Pitx2 provided evidence of key regulatory roles of this transcription factor during cardiogenesis and thus congenital heart diseases. More recently, impaired Pitx2 function has also been linked to arrhythmogenic processes, providing novel roles in the adult heart. In this manuscript, we provide a state-of-the-art review of the fundamental roles of Pitx2 during cardiogenesis, arrhythmogenesis and its contribution to congenital heart diseases.
Klasifikace
Druh
J<sub>ost</sub> - Ostatní články v recenzovaných periodicích
CEP obor
—
OECD FORD obor
30106 - Anatomy and morphology (plant science to be 1.6)
Návaznosti výsledku
Projekt
—
Návaznosti
I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace
Ostatní
Rok uplatnění
2017
Kód důvěrnosti údajů
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Údaje specifické pro druh výsledku
Název periodika
Journal of Cardiovascular Development and Disease
ISSN
2308-3425
e-ISSN
—
Svazek periodika
4
Číslo periodika v rámci svazku
4
Stát vydavatele periodika
CH - Švýcarská konfederace
Počet stran výsledku
19
Strana od-do
—
Kód UT WoS článku
—
EID výsledku v databázi Scopus
—