ArticleCell death discovery2023
Age-related elevation of O-GlcNAc causes meiotic arrest in male mice.
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 10 papers.
What it found
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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
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- Results of the first-in-human, randomized, double-blind, placebo-controlled, single- and multiple-ascending dose study of BIIB113 in healthy volunteers.The journal of prevention of Alzheimer's disease · 2025Trial
- Docosahexaenoic acid alleviates Ornidazole toxicity related to spermatogenic dysfunction by modulating PPARγ-dependent ER-mitochondrial uncoupling.Science China. Life sciences · 2026Article
- Normal spermatogenesis in older men is associated with compensatory transcriptome changes.GeroScience · 2026Article
- O-GlcNAc transferase governs spermatogenic mitotic-to-meiotic transition and progression by coordinating transcription and alternative splicing programs.Cellular & molecular biology letters · 2026Article
- TargetingbioRxiv : the preprint server for biology · 2025Article
- Protein O-GlcNAcylation in reproductive biology and the impact of metabolic disease.Human reproduction update · 2025Review
- Renal tubular GSDME protects cisplatin nephrotoxicity by impeding OGT-STAT3-S100A7A axis in male mice.Nature communications · 2025Article
- O-GlcNAcylation in Endocrinology: The Sweet Link.Endocrinology · 2025Review
- O-GlcNAc participates in the meiosis of aging oocytes by mediating mitochondrial function.Reproduction (Cambridge, England) · 2024Article
- Analyzing high-throughput assay data to advance the rapid screening of environmental chemicals for human reproductive toxicity.bioRxiv : the preprint server for biology · 2024Article
Corrections and comments
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Authors and funding
23 authors at 2 institutions in 1 country.
Funding
Abstract
In recent years, the postponement of childbearing has become a critical social issue. Male fertility is negatively associated with age because of testis aging. Spermatogenesis is impaired with age, but the molecular mechanism remains unknown. The dynamic posttranslational modification O-linked N-acetylglucosamine (O-GlcNAc), which is a type of monosaccharide modification, has been shown to drive the process of aging in various systems, but it has not yet been investigated in the testis and male reproductive aging. Thus, this study aims to investigate the alteration of O-GlcNAc with aging and explore the role of O-GlcNAc in spermatogenesis. Here, we demonstrate that the decline in spermatogenesis in aged mice is associated with elevation of O-GlcNAc. O-GlcNAc is specifically localized in differentiating spermatogonia and spermatocytes, indicating its crucial role in meiotic initiation and progression. Mimicking the age-related elevation of O-GlcNAc in young mice by disabling O-GlcNAcase (OGA) using the chemical inhibitor Thiamet-G can recapitulate the impairment of spermatogenesis in aged mice. Mechanistically, the elevation of O-GlcNAc in the testis leads to meiotic pachytene arrest due to defects in synapsis and recombination. Furthermore, decreasing O-GlcNAc in aged testes using an O-GlcNAc transferase (OGT) inhibitor can partially rescue the age-related impairment of spermatogenesis. Our results highlight that O-GlcNAc, as a novel posttranslational modification, participates in meiotic progression and drives the impairment of spermatogenesis during aging.
Identifiers
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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 Socratic graph.