ArticleCommunications biology2025
OTUB2/NR4A1 restrains the development of preeclampsia by suppressing macrophage M1 polarization.
Article in Communications biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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.
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Who cites it
3 citing papers in PubMed.
- Experimental Animal Models of Preeclampsia: Mechanisms, Strengths, and Translational Relevance.Arteriosclerosis, thrombosis, and vascular biology · 2026Review
- NR4A1 Regulates Glycolysis in M1 Macrophages via the Wnt/β-Catenin Pathway to Affect Sepsis-Induced Myocardial Injury.Journal of inflammation research · 2026Article
- Article
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Authors and funding
6 authors.
Funding
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Abstract
Preeclampsia is one of the most common pregnancy disorders, and characterized by insufficient trophoblast invasion and placental inflammation. Our RNA sequencing results showed that OTU deubiquitinase, ubiquitin aldehyde binding 2 (OTUB2) was downregulated in placenta from preeclampsia patients, compared with the healthy control. Clinical and experimental data demonstrated that OTUB2 was expressed in macrophages. Gain- and loss-of-function experiments revealed that OTUB2 overexpression blocked M1 polarization of macrophages, and attenuated macrophages-induced apoptosis, and impaired migration and invasion of trophoblasts. Moreover, OTUB2 alleviated LPS-induced preeclampsia-like symptoms in rats, including hypertension, proteinuria, inflammation in placenta and insufficient infiltration of trophoblasts. Additionally, OTUB2 mediated deubiquitination of nuclear receptor subfamily 4 group A member 1 (NR4A1) and suppressed its degradation, and the Cys51 is crucial for catalytic activity of OTUB2. The effects of OTUB2 were partially reversed by shNR4A1. In conclusion, OTUB2 suppressed macrophage M1 polarization, macrophages-induced trophoblast damage, and restrained experimental preeclampsia in rodents by mediating deubiquitination of NR4A1. These findings may provide novel insight for clinical prevention and diagnosis of preeclampsia.
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