ArticleBiogerontology2025
Histone lysine methyltransferases and their specific methylation marks show significant changes in mouse testes from young to older ages.
Article in Biogerontology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- KMT5a-Mediated IRF3 Stabilization Enhances Macrophage Chemotaxis and Renal Fibrosis Progression.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Sertoli cell aging: damage accumulation and epigenetic alterations affecting male fertility.Biogerontology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
Spermatogenesis is finely regulated by histone methylation, which is crucial for regulating gene expression and chromatin remodeling. Functional studies have demonstrated that the histone lysine methyltransferases (KMTs) SETD1B, CFP1, SETDB1, G9A, and SETD2 play pivotal roles in spermatogenesis through establishing the key histone methylation marks, H3K4me3, H3K9me2, H3K9me3, and H3K36me3, respectively. This study aimed to evaluate the spatiotemporal expression of these KMTs and methylation marks as well as senescence-associated β-galactosidase (β-GAL), transcriptional activity, and apoptosis rates in mouse testes during biological aging. In accordance with these purposes, the following groups of Balb/C mice were created: young (1- and 2-week-old), prepubertal (3- and 4-week-old), pubertal (5- and 6-week-old), postpubertal (16-, 18-, and 20-week-old), and aged (48-, 50-, and 52-week-old). The β-GAL staining gradually increased from the young to the aged groups (P < 0.01). The SETD1B, G9A, SETDB1, and SETD2 protein levels increased in spermatogonia, early and pachytene spermatocytes, and Sertoli cells of the aged group (P < 0.05). In contrast, CFP1 protein level decreased in spermatogonia, pachytene spermatocytes, round spermatids, and Sertoli cells towards the older ages (P < 0.05). Moreover, H3K4me3, H3K9me2, H3K9me3, and H3K36me3 levels increased in the aged group (P < 0.05). There was also a significant reduction in apoptosis rates in seminiferous tubules of the pubertal, postpubertal, and aged groups (P < 0.01). Consequently, accumulation of histone methylation marks due to increased expression of KMTs in spermatogenic and Sertoli cells during testicular aging may alter chromatin reprogramming and gene expression, contributing to age-related fertility loss.
Indexed as
Identifiers
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.