ArticleExperimental animals2025
Therapeutic potential of omentin-1 in preeclampsia: enhancing fetal outcomes, vascular function, and reducing inflammation.
Article in Experimental animals, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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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
4 citing papers in PubMed.
- Epigenome-wide DNA methylation and spontaneous preterm birth among pregnant black women.Clinical epigenetics · 2026Article
- The role of omentin-1 in female reproduction: a critical review.The Journal of reproduction and development · 2026Review
- Role of Adipokines Chemerin, Visfatin, and Omentin in Obesity and Their Inflammatory and Metabolic Implications.Biomedicines · 2025Review
- Omentin-General Overview of Its Role in Obesity, Metabolic Syndrome and Other Diseases; Problem of Current Research State.Biomedicines · 2025Review
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study evaluated the therapeutic potential of omentin-1 in preeclampsia (PE). A PE-like mouse model received recombinant human omentin-1 protein (rh-omentin) from gestation day (gd) 13.5 to 16.5. On gd 17.5, fetuses and placentas were weighed, and soluble fms-like tyrosine kinase-1 (sFlt-1) levels were measured. Maternal aortic rings were used for ex vivo vascular reactivity assays. Inflammatory factors and Krüppel-like factor 2 (KLF2) expression in placental and aortic tissues were assessed using qPCR. Human umbilical vein endothelial cells (HUVECs) were exposed to plasma from PE patients or healthy pregnant individuals to evaluate omentin-1 and KLF2 expression by qPCR, with additional evaluation of KLF2 after rh-omentin treatment. Rh-omentin treatment reduced blood pressure in the PE-like model, accompanying by increased fetal and placental weights and higher fetal/placental weight ratios compared to untreated PE mice. Additionally, rh-omentin enhanced endothelial function in maternal aortic rings, as well as reduced placental necrosis and promoted CD31-positive vasculature in the labyrinth zone. Moreover, rh-omentin decreased pro-inflammatory factors in aortic and placental tissues of PE mice. KLF2 expression was restored in both aortic and placental tissues of PE mice and in HUVECs exposed to PE plasma following rh-omentin treatment. Rh-omentin improved fetal and placental outcomes in PE-like mice, enhancing vascular function and reducing inflammation in aortic and placental tissues. It also restored KLF2 expression in PE tissues and HUVECs exposed to PE plasma, suggesting therapeutic potential for addressing endothelial dysfunction in PE.
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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 Socratic graph.