ReviewFrontiers in cell and developmental biology2021
Meiotic Recombination Defects and Premature Ovarian Insufficiency.
Review in Frontiers in cell and developmental biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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Who cites it
32 citing papers in PubMed, 1 synthesis or guideline pooled it, 71 citations in OpenAlex.
- Pharmacogenomic studies of fertility outcomes in pediatric cancer survivors - A systematic review.Clinical and translational science · 2024Pooled it
- Prenatal exposure to polystyrene nanoplastics impairs offspring fertility in mice by disrupting meiotic recombination and chromatin accessibility in oocytes.Archives of toxicology · 2026Article
- Two compound heterozygous MEIOSIN (likely) pathogenic variants cause female infertility with premature ovarian insufficiency through the disruption of meiosis-related gene transcription.Journal of ovarian research · 2026Article
- Ypel5 preserves female fertility by regulating folliculogenesis and oocyte maturation.Cell death and differentiation · 2026Article
- Mutation in MSH5 Causes Primary Ovarian Insufficiency and Successful Therapeutic Intervention by In Vitro Fertilisation.Journal of cellular and molecular medicine · 2026Article
- Mechanism and potential therapeutic strategies of genetic abnormalities involved in deoxyribonucleic acid double-strand breaks leading to the development of human non-obstructive azoospermia.Reproductive biology and endocrinology : RB&E · 2026Review
- Modeling mammalian meiosis with pluripotent stem cells: progress and challenges.Clinical epigenetics · 2026Review
- Review
- Genetic variants in diminished ovarian reserve and premature ovarian insufficiency: implications for assisted reproductive outcomes.Journal of assisted reproduction and genetics · 2025Article
- SWS1-complex in premature ovarian insufficiency: SWSAP1 as a new POI gene.Human reproduction (Oxford, England) · 2025Article
- CNTD1 is crucial for crossover formation in female meiosis and for establishing the ovarian reserve.The Journal of cell biology · 2025Article
- Biallelic BRCA2 variants induce premature ovarian insufficiency by impaired meiotic homologous recombination.Communications biology · 2025Article
- HELQ Maintains Genome Stability of Primordial Germ Cells by Inhibiting LINE-1 Expression.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Difference of the gut microbiota of premature ovarian insufficiency in two traditional Chinese syndromes.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2025Article
- Premeiotic deletion of Eif2s2 causes oocyte arrest at the early diplotene stage and apoptosis in mice.Cell proliferation · 2024Article
- Defects in meiosis I contribute to the genesis of androgenetic hydatidiform moles.The Journal of clinical investigation · 2024Article
- The role of RAD51 regulators and variants in primary ovarian insufficiency, endometriosis, and polycystic ovary syndrome.NAR molecular medicine · 2024Review
- The crosstalk between telomeres and DNA repair mechanisms: an overview to mammalian somatic cells, germ cells, and preimplantation embryos.Journal of assisted reproduction and genetics · 2024Review
- Improving diagnostic precision in primary ovarian insufficiency using comprehensive genetic and autoantibody testing.Human reproduction (Oxford, England) · 2024Article
- Primary ovarian insufficiency: update on clinical and genetic findings.Frontiers in endocrinology · 2024Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Premature ovarian insufficiency (POI) is the depletion of ovarian function before 40 years of age due to insufficient oocyte formation or accelerated follicle atresia. Approximately 1-5% of women below 40 years old are affected by POI. The etiology of POI is heterogeneous, including genetic disorders, autoimmune diseases, infection, iatrogenic factors, and environmental toxins. Genetic factors account for 20-25% of patients. However, more than half of the patients were idiopathic. With the widespread application of next-generation sequencing (NGS), the genetic spectrum of POI has been expanded, especially the latest identification in meiosis and DNA repair-related genes. During meiotic prophase I, the key processes include DNA double-strand break (DSB) formation and subsequent homologous recombination (HR), which are essential for chromosome segregation at the first meiotic division and genome diversity of oocytes. Many animal models with defective meiotic recombination present with meiotic arrest, DSB accumulation, and oocyte apoptosis, which are similar to human POI phenotype. In the article, based on different stages of meiotic recombination, including DSB formation, DSB end processing, single-strand invasion, intermediate processing, recombination, and resolution and essential proteins involved in synaptonemal complex (SC), cohesion complex, and fanconi anemia (FA) pathway, we reviewed the individual gene mutations identified in POI patients and the potential candidate genes for POI pathogenesis, which will shed new light on the genetic architecture of POI and facilitate risk prediction, ovarian protection, and early intervention for POI women.
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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.