Proceedings of the National Academy of Sciences of the United States of AmericaOct 6, 2026

Late-onset preeclampsia is linked to faster aging of the placenta

Longevity & Aging Weekly Brief ↗PubMed ↗DOI ↗OA ↗

Updated Oct 7, 2026

Abstract

Late-onset preeclampsia (LOPE) is associated with accelerated molecular aging in placentae, evidenced by telomere attrition and DNA damage.

Accelerated molecular aging in LOPE placentae is marked by telomere shortening and increased DNA damage.
Oxidative stress drives telomere shortening and disrupts the balance of blood vessel formation in the placenta.
Inflammation does not significantly affect the aging process of the placenta in the context of LOPE.
Antioxidant treatment with superoxide dismutase helps preserve telomere length, reduces DNA damage, and restores blood vessel formation.
Reduced expression of specific RNA molecules (TERRAs) is identified as a hallmark of LOPE.
Depletion of TERRAs through targeted treatment leads to worsened telomere erosion and cellular aging in placental cells.

Simplified

Late-onset preeclampsia (LOPE) is a major pregnancy complication characterized by hypertension and placental dysfunction, resolving only upon delivery. Here, we show that LOPE placentae undergo accelerated molecular aging, marked by telomere attrition, DNA damage, and trophoblast senescence. Using primary placental tissue and trophoblast organoids, we demonstrate oxidative stress as a driver of telomere shortening and angiogenic imbalance. Inflammation did not alter placental aging trajectories. Antioxidant treatment (superoxide dismutase) preserved telomere length, reduced DNA damage, and restored angiogenic balance, highlighting oxidative stress as a modifiable determinant of placental aging. We identify reduced expression of telomeric repeat-containing RNAs (TERRAs) as a molecular hallmark of LOPE, and show that antisense oligonucleotide-mediated TERRA depletion exacerbates telomere erosion and senescence. Together, these findings delineate oxidative stress and TERRA loss as mechanisms driving placental decline, establish trophoblast organoids as a tractable model of placental aging, and reveal potential therapeutic avenues for mitigating preeclampsia-associated placental dysfunction.

Full Text

Full text is available at the source.

View Full Text ↗

Late-onset preeclampsia is linked to faster aging of the placenta

Abstract

Full Text

You found one interesting study. We’ll send the next 7.

What Lands in Your Inbox Each Week:

Recent issues from the longevity & aging brief