Environmental challenges, such as maternal stress, can significantly affect fetal growth and health outcomes throughout life. While the full role of the placenta in mediating these effects is uncertain, studies have shown that the placental enzyme 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2), which catalyses the conversion of cortisone to cortisol, must play a key role.

Using mice lacking 11β-HSD2 to model maternal stress, Wyrwoll et al. explored its consequences for fetal cardiovascular development, and whether the effects are reversible. They found evidence that cardiovascular development was impaired in Hsd11b2^−/− fetuses; these didn’t experience the normal gestational increase in umbilical vein blood velocity or the decline in resistance index in the umbilical artery exhibited by their Hsd11b2^+/+ littermates. Evidence of fetal growth restriction and retarded heart development was also found. However, treatment with pravastatin improved all these parameters in Hsd11b2^−/− fetuses.

This suggests that statins may be useful therapeutically in addressing intrauterine growth retardation due to placental vascular hypofunction, but it remains to be seen whether these effects translate to humans.

Read the full article in Proceedings of the National Academy of Sciences of the USA doi:10.1073/pnas.1520356113