ReviewInternational journal of molecular sciences2023
Selected Genetic Factors Associated with Primary Ovarian Insufficiency.
Review in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 2 of them syntheses that pooled 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.
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
26 citing papers in PubMed, 2 syntheses or guidelines pooled it, 59 citations in OpenAlex.
- Performance of exome sequencing in premature ovarian insufficiency: a systematic review and meta-analysis.BMC pregnancy and childbirth · 2026Pooled it
- Reduced ovarian reserve among female offspring of consanguineous marriages in the Middle East-a mini review.Frontiers in reproductive health · 2025Pooled it
- Imeglimin halts cyclophosphamide-induced ovarian injury: a dual modulation of TLR4/NF-κB/NLRP3-driven inflammation and AMPK/SIRT1/PGC-1α pathways.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Bioengineering Ovarian Endocrine Function: From Follicle Modeling to Cell-Based Hormone Therapy.Advanced healthcare materials · 2026Review
- STAG3 c.2776C > T, p.Arg926Ter is a recurrent variant in Russian patients with early-onset premature ovarian insufficiency.Journal of assisted reproduction and genetics · 2026Article
- A Novel BIRC6 Variant Impairs Apoptotic Regulation in Familial Premature Ovarian Insufficiency: Functional Validation in a CRISPR/Cas9 Zebrafish Model.Reproductive sciences (Thousand Oaks, Calif.) · 2026Article
- Identification of cryosensitive niches and a targetable FOS/AP‑1 program in the human ovarian cortex by single‑cell and spatial transcriptomics.BMC medicine · 2026Article
- USP9X as a Candidate Mediator of Prenatal Aspirin-Induced Ovarian Reserve Reduction in Offspring Mice.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Oocyte-specific knockout of eIF2 subunits causes apoptosis of mouse oocytes within the early growing follicles via mitochondrial dysfunctions and DNA damage.Cell death & disease · 2026Article
- Meiotic gene expression ofInternational journal of reproductive biomedicine · 2026Article
- Recent advances in methods for establishing animal models of premature ovarian failure.Journal of ovarian research · 2025Review
- Noninvasive markers for warning premature ovarian insufficiency: a Mendelian randomisation study.Journal of ovarian research · 2025Article
- Functional analysis of 6 variations inSAGE open medicine · 2025Article
- Premeiotic deletion of Eif2s2 causes oocyte arrest at the early diplotene stage and apoptosis in mice.Cell proliferation · 2024Article
- An overview of different methods to establish a murine premature ovarian failure model.Animal models and experimental medicine · 2024Review
- Population-based FMR1 carrier screening among reproductive women.Journal of assisted reproduction and genetics · 2024Article
- Genetic insights into the complexity of premature ovarian insufficiency.Reproductive biology and endocrinology : RB&E · 2024Review
- Review
- TP63 truncating mutation causes increased cell apoptosis and premature ovarian insufficiency by enhanced transcriptional activation of CLCA2.Journal of ovarian research · 2024Article
- A Human HomozygousGenes · 2024Article
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 at 1 institution in 1 country.
Funding
Abstract
Primary ovarian insufficiency (POI) is a heterogeneous disease resulting from non-functional ovaries in women before the age of 40. It is characterized by primary amenorrhea or secondary amenorrhea. As regards its etiology, although many POI cases are idiopathic, menopausal age is a heritable trait and genetic factors play an important role in all POI cases with known causes, accounting for approximately 20% to 25% of cases. This paper reviews the selected genetic causes implicated in POI and examines their pathogenic mechanisms to show the crucial role of genetic effects on POI. The genetic factors that can be found in POI cases include chromosomal abnormalities (e.g., X chromosomal aneuploidies, structural X chromosomal abnormalities, X-autosome translocations, and autosomal variations), single gene mutations (e.g., newborn ovary homeobox gene (NOBOX), folliculogenesis specific bHLH transcription factor (FIGLA), follicle-stimulating hormone receptor (FSHR), forkhead box L2 (FOXL2), bone morphogenetic protein 15 (BMP15), etc., as well as defects in mitochondrial functions and non-coding RNAs (small ncRNAs and long ncRNAs). These findings are beneficial for doctors to diagnose idiopathic POI cases and predict the risk of POI in women.
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What Socratic 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 Socratic graph.