ArticleJournal of perinatal medicine2025
Upregulation of microRNA-3687 promotes gestational diabetes mellitus by inhibiting follistatin-like 3.
Article in Journal of perinatal medicine, 2025. 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
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesPregnancy-related medical complications such as gestational diabetes mellitus (GDM) are common and associated with several obstetric and neonatal problems. There is growing evidence that microRNAs (miRNAs) are essential players in the pathophysiology of GDM. This study aimed to assess how particular miRNAs and the genes they target are expressed in GDM.
methodsA GDM cell model was created using BeWo cells cultured in hyperglycemic (HG) conditions (25 mM glucose). Low-glucose (LG) conditions (5.5 mM glucose) were used for the BeWo cells in the control group. Differentially expressed genes (DEGs) in BeWo cells were identified by high-throughput sequencing and their levels verified in placental samples from GDM patients and controls using RT-PCR. Furthermore, the target genes of the DEGs were verified using dual-luciferase reporter assays.
resultsHigh-throughput sequencing revealed 220 DEGs in BeWo cells. Among these, miR-3687 was significantly upregulated, while follistatin-like 3 (FSTL3) was downregulated in BeWo cells under HG conditions. The high-throughput sequencing results were corroborated by RT-PCR, which showed that placental samples from GDM patients had significantly lower levels of FSTL3 expression and substantially higher amounts of miR-3687 expression compared to control samples. FSTL3 was established as a direct target of miR-3687 as shown by dual-luciferase reporter assays.
conclusionsThe increase of miR-3687 might facilitate the onset and advancement of GDM by suppressing FSTL3. This discovery offered a new perspective on the molecular underpinnings of GDM and indicated possible targets for therapeutic intervention.
Indexed as
Identifiers
40219801What 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.