ArticleCell proliferation2015
Impaired proliferation of pancreatic beta cells, by reduced placental growth factor in pre-eclampsia, as a cause for gestational diabetes mellitus.
Article in Cell proliferation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
6 citing papers in PubMed, 1 synthesis or guideline pooled it, 12 citations in OpenAlex.
- Metabolic abnormalities and obesity's impact on the risk for developing preeclampsia.American journal of physiology. Regulatory, integrative and comparative physiology · 2017Pooled it
- NRF2 deficiency leads to inadequate beta cell adaptation during pregnancy and gestational diabetes.Redox biology · 2025Article
- Associations between first-trimester screening biomarkers and maternal characteristics with gestational diabetes mellitus in Chinese women.Frontiers in endocrinology · 2024Article
- Exploring the causes and consequences of maternal metabolic maladaptations during pregnancy: Lessons from animal models.Placenta · 2020Review
- Effects of miR‑195‑5p on cell proliferation and apoptosis in gestational diabetes mellitus via targeting EZH2.Molecular medicine reports · 2020Article
- Reduction in placental growth factor impaired gestational beta-cell proliferation through crosstalk between beta-cells and islet endothelial cells.American journal of translational research · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesReduced increase in serum placental growth factor (PLGF) levels frequently occurs in patients with pre-eclampsia (PE) and thus has been used as a predictive factor for developing PE. However, it has remained elusive how shortage of PLGF could affect pancreatic endocrine homoeostasis and function in pregnancy to lead to development of gestational diabetes mellitus (GDM). MATERIALS AND
methodsWe used l-NAME injection in mice, as a model of human PE, in which PLGF levels were significantly reduced.
resultsWe not only confirmed reduced serum PLGF levels in patients with PE but also detected strong correlation of serum PLGF levels and presence of GDM. We found that growth of beta cell mass during pregnancy was significantly impaired by l-NAME injection, as a result of reduced beta cell proliferation. This may explain the higher risk of developing GDM in patients with PE. Moreover, provision of exogenous PLGF in l-NAME-treated pregnant mice significantly rescued beta cell proliferation, with subsequent increase in beta cell mass, suggesting that shortage in PLGF may be responsible for impaired beta cell growth and higher occurrence of GDM in patients with PE.
conclusionsOur study highlighted a pivotal role for PLGF in prevention and treatment of GDM in patients with 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 OpenQuestion graph.