Evidence mapPaperPMID 40790236Full record

ArticleGenomics & informatics2025

Unravelling the molecular landscape of polycystic ovary syndrome (PCOS) and role of inflammation through transcriptomics analysis of human ovarian granulosa cells.

Kanika Mahra, Vineet Singh, Jae-Ho Shin

Abstract read
In one paragraph

Article in Genomics & informatics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Review
  2. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors.

Kanika Mahra *Department of Applied Biosciences, Kyungpook National University, Daegu, 41566, Republic of Korea.ORCID http://orcid.org/0009-0000-6826-6719
Vineet Singh *Department of Applied Biosciences, Kyungpook National University, Daegu, 41566, Republic of Korea.ORCID http://orcid.org/0000-0003-2458-3282
Jae-Ho ShinDepartment of Applied Biosciences, Kyungpook National University, Daegu, 41566, Republic of Korea. jhshin@knu.ac.kr.ORCID http://orcid.org/0000-0001-6450-9787

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPolycystic ovary syndrome (PCOS) is a common metabolic problem in women of reproductive age that can lead to infertility and other metabolic disorders. Recent evidence indicates that inflammation might be one of the contributing factors in PCOS progression. However, there is a lack of information on the regulation of inflammatory genes in PCOS. Therefore, the aim of the study is to investigate the role of inflammation-associated genes and pathways in relation to PCOS.

methodThe bulk RNA-seq data of granulosa cells of human ovaries of PCOS-affected and healthy women were analyzed to evaluate the inflammatory regulation in PCOS. After quality trimming, the raw RNA-seq data were aligned to the human genome, and gene expression was quantified using featureCounts with Ensembl annotation. Further, downstream analyses of the resulting count matrix were performed in R Studio, where differentially expressed genes (DEG) were identified and CO-DEG analysis was performed.

resultsThe study identifies the various differentially expressed inflammatory genes in the case of PCOS such as SPI1, HSPB1, MNDA, and ITGA. These DEG are closely associated with the activation of inflammatory responses, i.e., activation of lymphocytes and leukocytes, leukocyte migration and mononuclear cell proliferation, stimulating binding of various cytokines, immunoglobulins, and chemokines. PCOS group also exhibited an increased expression of androgen-mediated genes (SPI1 and ETS transcription factors) and genes associated with hyperlipidemia and insulin resistance (TNFRSF1B). Further, KEGG pathway enrichment analysis revealed significant upregulation of various pathways (autophagy, endocytosis) in the PCOS group. In addition, network analysis (cnetplot) of the top 10 KEGG GSEA pathways also highlights the key pathways in the PCOS group such as SNARE complex assembly pathway, SNAP-25, nucleophagy, and regulation of mast cell activation.

conclusionTherefore, the study highlights that inflammation is a major effector in PCOS, which also fuels obesity, an independent effector that further worsens the PCOS condition. In addition, the genes related to hyperandrogenism, hyperlipidemia, and insulin resistance were also overexpressed in PCOS, exacerbating the condition.

Indexed as

Granulosa cellsInflammationObesityPCOSRNA-seq

Identifiers

PMID40790236
PMCPMC12337442

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.