Evidence map›Paper›PMID 40116548›Full record

ReviewPhysiological research2025

Mechanisms of Granulosa Cell Programmed Cell Death and Follicular Atresia in Polycystic Ovary Syndrome.

Y-H Shen, S Peng, T Zhu, M-J Shen

Abstract readReview
In one paragraph

Review in Physiological research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing 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

18 citing papers in PubMed.

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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

4 authors.

Y-H ShenDepartment of Gynecology, Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai, China. shen_mj2564@126.com and tingzhuzhtia@126.com.
S Peng
T Zhu
M-J Shen

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Polycystic ovary syndrome (PCOS) is a common endocrine disorder affecting women of reproductive age, characterized by a spectrum of reproductive, endocrine, and metabolic disturbances. The etiology of PCOS encompasses a complex interplay of genetic, metabolic, inflammatory, and oxidative factors, though the precise pathological mechanisms remain inadequately understood. Despite considerable variability in the clinical characteristics and biochemical profiles among individuals with PCOS, abnormalities in follicular development are a hallmark of the condition. Granulosa cells, integral to follicular development, play a pivotal role in follicle maturation. Recent studies have established a strong correlation between granulosa cell programmed cell death and follicular atresia in PCOS. This review provides a comprehensive analysis of the current understanding of granulosa cell programmed cell death and its contribution to follicular atresia within the pathophysiology of PCOS, providing a foundation for future research endeavors. Key words Follicular atresia, Hyperandrogenism, Insulin resistance, Polycystic ovary syndrome, Programmed cell death of granulosa cells.

Indexed as

ApoptosisFollicular AtresiaGranulosa CellsPolycystic Ovary SyndromeAnimalsFemaleHumansInsulin Resistance

Identifiers

PMID40116548
PMCPMC11995941

What OpenQuestion holds

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Registered trials

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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.