ReviewPhysiological genomics2022
Linking inflammatory adipose tissue to placental abnormalities in obese preeclamptic pregnancies.
Review in Physiological genomics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- Adipokines in preeclampsia: disrupted signaling pathways and novel therapeutic strategies.European journal of medical research · 2025Review
- Extracellular vesicle-associated miR-515-5p from adipose tissue regulates placental metabolism and fetal growth in gestational diabetes mellitus.Cardiovascular diabetology · 2025Article
- Pathophysiology of Maternal Obesity and Hypertension in Pregnancy.Journal of cardiovascular development and disease · 2025Review
- Early pregnancy cardiometabolic index and its association with hypertensive disorder complicating pregnancy.American journal of translational research · 2025Article
- Position statement of Italian Society of Obesity (SIO): Gestational Obesity.Eating and weight disorders : EWD · 2024Review
- The Role of Obesity in the Development of Preeclampsia.Current hypertension reports · 2024Review
- Relationship Between Cardiometabolic Index in Early Pregnancy and Hypertensive Disorder Complicating Pregnancy.Cureus · 2024Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Preeclampsia (PE), a pregnancy-specific disorder, is characterized by maternal hypertension and proteinuria or another accompanying sign/symptom of multiorgan dysfunction. Maternal symptoms resolve with delivery of the baby and, importantly, the placenta. Therefore, the placenta plays a causal role in PE. However, the precise cause of abnormal placental development and/or function is unknown. Women with obesity have an increased risk of developing PE that is potentially related to the increased inflammation that accompanies increased maternal adiposity. Furthermore, inflammatory adipokines, i.e., leptin, have been linked to the development of systemic inflammation, hypertension, and other adverse outcomes associated with PE. Rodent models that recapitulate key pathophysiological features of the maternal and fetal syndrome have been used translationally to study PE. This review covers inflammatory adipokines, immune cells, and impaired placental development associated with PE in women and in rodent models of PE that use functional genomics to test causation.
Indexed as
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.