The placenta ages as pregnancy advances, yet its continued function is required for a successful pregnancy outcome. Placental aging is a physiological phenomenon; however, there are some placentas that show signs of aging earlier than others. Premature placental senescence and aging are implicated in a number of adverse pregnancy outcomes, including fetal growth restriction, preeclampsia, spontaneous preterm birth, and intrauterine fetal death. Here we discuss cellular senescence, a state of terminal proliferation arrest, and how senescence is regulated. We also explore the role of physiological placental senescence and how aberrant placental senescence alters placental function, contributing to the pathophysiology of fetal growth restriction, preeclampsia, spontaneous preterm labor/birth, and unexplained fetal death.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1016/j.ajog.2017.11.567 | DOI Listing |
Am J Reprod Immunol
January 2025
Department of Medicine, Section of Infectious Diseases, Baylor College of Medicine, Houston, Texas, USA.
Problem: COVID-19 during pregnancy is linked to increased maternal morbidity and a higher incidence of preterm births (PTBs), yet the underlying mechanisms remain unclear. Cellular senescence, characterized by the irreversible cessation of cell division, is a critical process in placental function, and its dysregulation has been implicated in pregnancy complications like PTB. Senescence can be induced by various stressors, including oxidative stress, DNA damage, and viral infections.
View Article and Find Full Text PDFFundam Res
November 2024
National Clinical Research Center for Child Health and Disorder, Children's Hospital of Chongqing Medical University, Chongqing 401122, China.
The rising rates of pregnancies associated with advanced maternal age (AMA) have created unique challenges for healthcare systems worldwide. The elevated risk of poor maternal outcomes among AMA pregnancies is only partially understood and hotly debated. Specifically, AMA is associated with reduced fertility and an increased incidence of pregnancy complications.
View Article and Find Full Text PDFSci Rep
December 2024
Laboratory of Molecular and Cellular Immunology, Institute of Molecular Biology NAS RA, 7 Hasratyan Str., Yerevan, 0014, Armenia.
Antiphospholipid syndrome (APS) is associated with recurrent pregnancy morbidity, yet the underlying mechanisms remain elusive. We performed multifaceted characterization of the biological and transcriptomic signatures of mouse placenta and uterine natural killer (uNK) cells in APS. Histological analysis of APS placentas unveiled placental abnormalities, including disturbed angiogenesis, occasional necrotic areas, fibrin deposition, and nucleated red blood cell enrichment.
View Article and Find Full Text PDFFree Radic Res
December 2024
Department of Obstetrics and Gynecology, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu 610072, China.
This research investigates the interplay between Reactive Oxygen Species (ROS) and Apelin (APLN) in regulating autophagy, with implications for placental cell senescence and apoptosis in pre-eclampsia (PE). We manipulated APLN expression using sgRNA to study its effects on ROS levels and subsequent cellular responses. Our findings reveal that APLN overexpression elevates ROS production, accelerating cellular senescence and apoptosis.
View Article and Find Full Text PDFPlacenta
December 2024
Department of Animal Sciences, University of Florida, Gainesville, USA. Electronic address:
Introduction: Maternal hyperthermia (i.e. heat stress) can adversely affect placental development and function, with severity varying based on pregnancy stage.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!