ArticleCell death discovery2023
The EZH2-H3K27me3 axis modulates aberrant transcription and apoptosis in cyclophosphamide-induced ovarian granulosa cell injury.
Article in Cell death discovery, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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
12 citing papers in PubMed, 6 citations in OpenAlex.
- Age-associated chromatin repression of Hippo-Yap signaling drives oogonial stem cell decline in chicken.Functional & integrative genomics · 2026Article
- NADPH oxidases in immunometabolism and disease pathology: mechanistic networks, pollutant triggers, and therapeutic frontiers.Cellular & molecular immunology · 2026Review
- JMJD3-driven epigenetic reprogramming of p16Bone research · 2026Article
- HucMSC-mediated stromal metabolic reprogramming in reactivating aged ovaries: a single-cell transcriptomic perspective.Cellular & molecular biology letters · 2026Article
- Epigenetic deciphering of ovarian aging: multilayer interactive mechanisms and targeted reversal strategies.Epigenetics & chromatin · 2026Review
- Integrated network toxicology and multi-omics profiling reveal cell cycle, DNA damage repair, and metabolic alterations in cyclophosphamide-induced premature ovarian insufficiency.Frontiers in pharmacology · 2026Article
- Oxidoreductase delivery by cell therapies in cyclophosphamide-induced premature ovarian insufficiency: a mechanistic insight into ovarian rejuvenation.Journal of ovarian research · 2025Article
- Mechanism of crosstalk between DNA methylation and histone acetylation and related advances in diagnosis and treatment of premature ovarian failure.Epigenetics · 2025Review
- Managing the negative regulation of Sirtuins in a murine model of premature ovarian failure: focusing on the key roles of antioxidants.Journal of ovarian research · 2025Review
- Bushen Jianpi Tiaoxue Decoction (BJTD) inhibits the LIF-mTOR signaling axis to regulate mitochondrial function and alleviate cyclophosphamide-induced diminished ovarian reserve.Apoptosis : an international journal on programmed cell death · 2025Article
- Mesenchymal stem cells derived from hPSC via neural crest attenuate chemotherapy-induced premature ovarian insufficiency by ameliorating apoptosis and oxidative stress in granulosa cells.Stem cell research & therapy · 2025Article
- Protective effect of ginseng extract and total ginsenosides on hematopoietic stem cell damage by inhibiting cell apoptosis and regulating the intestinal microflora.International journal of molecular medicine · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chemotherapy-induced ovarian damage and infertility are significant concerns for women of childbearing age with cancer; however, the underlying mechanisms are still not fully understood. Our study has revealed a close association between epigenetic regulation and cyclophosphamide (CTX)-induced ovarian damage. Specifically, CTX and its active metabolite 4-hydroperoxy cyclophosphamide (4-HC) were found to increase the apoptosis of granulosa cells (GCs) by reducing EZH2 and H3K27me3 levels, both in vivo and in vitro. Furthermore, RNA-seq and CUT&Tag analyses revealed that the loss of H3K27me3 peaks on promoters led to the overactivation of genes associated with transcriptional regulation and apoptosis, indicating that stable H3K27me3 status could help to provide a safeguard against CTX-induced ovarian damage. Administration of the H3K27me3-demethylase inhibitor, GSK-J4, prior to CTX treatment could partially mitigate GC apoptosis by reversing the reduction of H3K27me3 and the aberrant upregulation of specific genes involved in transcriptional regulation and apoptosis. GSK-J4 could thus potentially be a protective agent for female fertility when undergoing chemotherapy. The results provide new insights into the mechanisms for chemotherapy injury and future clinical interventions for fertility preservation.
Identifiers
What 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.