Key result
Maternal autoantibodies directed to the p200 epitope of Ro52 correlate with fetal AV block and directly bind cardiomyocytes, dysregulating calcium homeostasis and inducing apoptosis.
Why the study?
Do maternal autoantibodies directed to the p200 epitope of Ro52 cause congenital heart block by dysregulating calcium homeostasis?
Do maternal autoantibodies directed to the p200 epitope of Ro52 cause congenital heart block by dysregulating calcium homeostasis?
The study identifies the cellular mechanism of congenital heart block, demonstrating that maternal p200 autoantibodies disrupt calcium homeostasis and induce apoptosis in cardiomyocytes.
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Hypothesis-generating for p200-targeted therapies in fetal AV block; human studies required before clinical consideration.
Salomonsson et al. (2005) studied Congenital heart block. Maternal autoantibodies directed to p200 of Ro52 protein was evaluated on Prolongation of fetal atrioventricular (AV) time and heart block, and cellular Ca2+ dysregulation. Maternal autoantibodies directed to the p200 epitope of Ro52 correlate with fetal AV block and directly bind cardiomyocytes, dysregulating calcium homeostasis and inducing apoptosis.
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