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

ABSTRACT:

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.

Methods

The study used clinical samples and two distinct mouse models of ICP to validate BACH1 alterations in ICP through immunohistochemistry (IHC), immunofluorescence (IF), and western blot (WB) analyses. Subsequently, global BACH1-knockout mice were employed to investigate the phenotypic effects of BACH1 deficiency on ICP progression. The molecular mechanisms underlying the regulatory role of BACH1 in ICP were further elucidated using mu

SUBMITTER: Li S 

PROVIDER: S-EPMC12044804 | biostudies-literature | 2025 May

REPOSITORIES: biostudies-literature