ArticleJournal of endocrinological investigation2026
lncRNA PANDAR predicts adverse pregnancy outcomes and reflects hyperglycemia-associated cellular stress in gestational diabetes mellitus.
Article in Journal of endocrinological investigation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
purposeGestational diabetes mellitus (GDM) is a common metabolic disorder of pregnancy associated with placental dysfunction and adverse maternal-fetal outcomes. LncRNAs have emerged as important regulators in metabolic diseases. The clinical significance and molecular mechanisms of lncRNA PANDAR in GDM remain unclear.
methods117 GDM patients and 110 healthy pregnant women were enrolled. Relative expression of genes was measured by qRT-PCR. The diagnostic value of PANDAR was assessed using ROC analysis, and its association with adverse pregnancy outcomes was evaluated by logistic regression. High-glucose model was established in HTR-8/Svneo trophoblast cells to investigate the function of PANDAR. Cell apoptosis, viability, and invasion were assessed using flow cytometry, CCK-8, and Transwell assays. The regulatory relationships among molecules were validated by dual-luciferase reporter assays.
resultsPANDAR expression was upregulated in GDM patients and exhibited good diagnostic performance. PANDAR levels were higher in GDM patients with adverse pregnancy outcomes. Elevated PANDAR was independently associated factor for adverse pregnancy outcomes. High glucose induced PANDAR expression and promoted trophoblast apoptosis while inhibiting cell viability and invasion, effects that were alleviated by PANDAR silencing. PANDAR functioned as a ceRNA for miR-192-5p, thereby upregulating the pro-apoptotic target BCL2L11. Rescue experiments confirmed that a PANDAR/miR-192-5p/BCL2L11 axis mediated trophoblast dysfunction under hyperglycemic conditions.
conclusionPANDAR is associated with adverse pregnancy outcomes and may reflect hyperglycemia-induced cellular responses by promoting trophoblast dysfunction via a miR-192-5p/BCL2L11 axis.
Indexed as
Identifiers
42400754What 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.