Elevated microRNA-187 causes cardiac endothelial dysplasia to promote congenital heart disease through inhibition of NIPBL.

The findings establish the miR-187/NIPBL axis as a potent regulator that inhibits cardiac endothelial cell development by attenuating the transcription of numerous endothelial genes, with the study's mouse and human cardiac organoid models effectively replicating severe defects from minor perturbations.

Countstar Castor S1 supported assessment of flow-cytometry cell measurements in the study's cell samples during migration assessment in the 2024 The Journal of clinical investigation study.