Placentas showed faster molecular aging in late-onset preeclampsia

Researchers studied primary placental tissue and trophoblast organoids, lab-grown models made from cells that help form the placenta. They examined late-onset preeclampsia, a pregnancy complication involving high blood pressure and placental dysfunction. Affected placentas showed accelerated molecular aging, with DNA damage and shortened telomeres, the protective ends of chromosomes. Placental cells also showed senescence, a state in which cells stop dividing.

Experiments using tissue and organoids identified oxidative stress, stress caused by reactive oxygen molecules, as a driver of telomere shortening and an imbalance in blood-vessel growth signals. The antioxidant enzyme superoxide dismutase preserved telomere length, reduced DNA damage and restored this balance. Inflammation did not alter placental aging patterns. Levels of telomere-associated RNA molecules were also lower in affected placentas. Experimentally reducing these molecules worsened telomere erosion and senescence.