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Peer-reviewedCC BY-NC-NDProceedings of the National Academy of Sciences of the United States of America

Late-onset preeclampsia is characterized by accelerated placental aging.

  • Anya L Arthurs1,2,3
  • Rudrarup Bhattacharjee3,4
  • Melanie D Smith1,2
  • Dulce L Medina Garcia4
  • Ellen Menkhorst5,6
  • German Mora4
  • Jessica M Williamson1,2
  • Lynda K Harris7
  • Jose M Polo4
  • David A MacIntyre3,4
  • Claire T Roberts1,2
7 affiliations
  1. 1Discipline of Women's and Children's Health, Flinders Health and Medical Research Institute, Flinders University, Adelaide, SA 5042, Australia.
  2. 2College of Medicine and Public Health, Flinders University, Adelaide, SA 5042, Australia.
  3. 3Robinson Research Institute, University of Adelaide, Adelaide, SA 5000, Australia.
  4. 4Adelaide Centre for Epigenetics, School of Biomedicine, and South Australian Immunogenomics Cancer Institute, University of Adelaide, Adelaide, SA 5000, Australia.
  5. 5Department of Obstetrics, Gynaecology and Newborn Health, University of Melbourne, Parkville, VIC 3010, Australia.
  6. 6Gynaecology Research Centre, Royal Women's Hospital, Parkville, VIC 3052, Australia.
  7. 7Department of Obstetrics and Gynaecology, University of Nebraska Medical Center, Omaha, NE 68198.
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Abstract

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.

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Cite

BibTeXRIS
BibTeX
@article{arthurs2026lateonset,
  title = {{Late-onset preeclampsia is characterized by accelerated placental aging.}},
  author = {Anya L Arthurs and Rudrarup Bhattacharjee and Melanie D Smith and Dulce L Medina Garcia and Ellen Menkhorst and German Mora and Jessica M Williamson and Lynda K Harris and Jose M Polo and David A MacIntyre and Claire T Roberts},
  journal = {Proceedings of the National Academy of Sciences of the United States of America},
  year = {2026},
  month = oct,
  doi = {10.1073/pnas.2614827123},
  url = {https://europepmc.org/article/MED/42837445},
  note = {CC BY-NC-ND},
}
RIS
TY  - JOUR
TI  - Late-onset preeclampsia is characterized by accelerated placental aging.
AU  - Anya L Arthurs
AU  - Rudrarup Bhattacharjee
AU  - Melanie D Smith
AU  - Dulce L Medina Garcia
AU  - Ellen Menkhorst
AU  - German Mora
AU  - Jessica M Williamson
AU  - Lynda K Harris
AU  - Jose M Polo
AU  - David A MacIntyre
AU  - Claire T Roberts
PY  - 2026
DA  - 2026/10/06
JO  - Proceedings of the National Academy of Sciences of the United States of America
DO  - 10.1073/pnas.2614827123
UR  - https://europepmc.org/article/MED/42837445
AB  - 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.
SN  - 0027-8424
SN  - 1091-6490
ER  -