During normal embryonic heart development, muscle cells migrate and proliferate, forming finger-like protrusions inside the cardiac chamber. The projections, called trabeculae, help with heart nutrition and oxygenation until blood vessels form. They eventually dissolve, leading to the formation of a compact, smooth and solid heart wall. In some embryos, however, the trabeculae fail to dissolve and form solid heart wall, leading to LVNC, in which the trabeculae project into a thinned lower left heart chamber.
"LVNC is one of the most common disorders in cardiac chamber maturation. People born with this condition often do not experience any symptoms, but can be at higher risk of heart failure, irregular heart rhythms, or sudden cardiac arrest," said Assistant Professor Manvendra Singh, from Duke-NUS' Cardiovascular and Metabolic Disorders (CVMD) Programme, the senior and corresponding author of the study.
Scientists - Understanding - Changes - LVNC - Asst
Globally, scientists' understanding of the molecular and genetic changes that lead to LVNC is limited. Asst Prof Singh and his colleagues in Singapore, Japan, and the USA wanted to test if a particular protein, Sema3E, is linked to the defects seen in LVNC. Sema3E is known to connect with a cell receptor, called PlexinD1, which is involved in embryonic heart development. However, Sema3E's existence in the heart had not yet been determined.
The team first turned off Plxnd1, the gene that codes for the PlexinD1 receptor, in a preclinical model of embryo hearts. This...
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