It has been observed that maternal autoantibodies can be transported across the placenta, and they may affect the developing fetus and contribute to the development of fetal CHB.[16] Regarding the molecular mechanisms leading to CAVB, several hypotheses have been proposed in the literature, but none of the proposed model was capable of explaining all aspects of CHB.[16],[17] A relatively well-accepted model is that anti-Ro52 antibody may directly affect calcium homeostasis in the fetal heart, leading to disturbances in signal conduction and/or
electrogenesis. In addition, deposition of maternal antibodies was found in the heart of fetuses who died of CHB.
Devor, "Membrane potential oscillations in dorsal root ganglion neurons: role in normal
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