Fig 2: In vivo inhibition of FKBP5 mitigates aPLs-induced maternal‒fetal interface damage. (A) Schematic diagram of the experimental protocol for constructing the NP, OAPS, and OAPS + SAFit2 mouse models. (B–E) Representative images of E14.5 uterine morphology in the NP, OAPS and OAPS + SAFit2 groups of mice. FRF, mean fetal weight and mean placental weight were compared among the three groups of model mice. (F) Representative photographs of uterine morphology and histologic analysis of placentas from the NP, OAPS, and OAPS + SAFit2 groups. The white arrows indicate instances of stillbirths, placental hematomas, and fetal growth restriction in mice or areas of necrotic placental tissue and diseased blood vessels. (G–I) IF showing changes in the expression of iNOS and Arg-1 at the placental interface among the NP, OAPS, and OAPS + SAFit2 groups, which were statistically analyzed. Scale bar = 20 μm. (J‒L) Representative IF images of E-cadherin and Vimentin at the placental interface across the NP, OAPS, and OAPS + SAFit2 groups, which were statistically analyzed. Scale bar = 50 μm. (M) IHC revealed altered localization and expression of pJAK1, pSTAT1, PPARγ, and pSTAT6 at the placental interface in the NP, OAPS, and OAPS + SAFit2 groups of mice. Scale bar = 100 μm. The data are shown as the means ± SEMs. *P < 0.05, **P < 0.01, ***P < 0.001.