BACH1 deficiency improves placental angiogenesis via SLC25A51-mediated mitochondrial NAD transport in intrahepatic cholestasis of pregnancy.

Background: Placental angiogenesis is particularly important in the treatment of intrahepatic cholestasis of pregnancy (ICP). Although BACH1 has been implicated in angiogenesis associated with cardiovascular diseases, its specific role and underlying mechanisms in ICP remain unclear. This study aims to investigate the role of BACH1 in ICP.

Preconception maternal hyperoxia exposure causes cardiac insufficiency through induction of mitochondrial toxicity in mice offspring.

Although essential, excessive oxygen is toxic. The adverse effects of maternal hyperoxygenation have recently garnered attention. However, the potential toxicity of maternal hyperoxia exposure before pregnancy and its effects on offspring development remain unclear.