ReviewMolecular medicine reports2026
Role of ubiquitin‑proteasome system in preeclampsia (Review).
Review in Molecular medicine reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Targeting the GSK-3β/mTOR axis: a novel pharmacological strategy for preeclampsia prevention and treatment.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Epigenetic mechanisms in preeclampsia: translational therapeutic strategies and precision-medicine perspectives.Journal of medicine and life · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Preeclampsia (PE) is a multifactorial pregnancy disorder characterized by hypertension and proteinuria, primarily resulting from placental abnormalities and endothelial dysfunction. The present review explores the role of ubiquitination and deubiquitination (key post‑translational modifications), in the pathogenesis of PE. Ubiquitination, catalyzed by E1, E2 and E3 enzymes, and reversed by deubiquitinating enzymes, regulates protein stability and function, thereby influencing key cellular processes in trophoblasts. Dysregulation of these pathways impairs trophoblast functions and contributes to PE development. In addition, the present review discusses emerging therapeutic strategies targeting the ubiquitin‑proteasome system, including deubiquitinase‑targeting chimera and proteolysis‑targeting chimeras. Targeting ubiquitination and deubiquitination mechanisms presents a promising avenue for the treatment of PE. Further research into these pathways may lead to novel interventions aimed at improving maternal and fetal outcomes.
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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.