Evidence map›Paper›PMID 39891142›Full record

ArticleCell communication and signaling : CCS2025

Ionizing radiation-induced disruption of Rela-Bclaf1-spliceosome regulatory axis in primary spermatocytes causing spermatogenesis dysfunction.

Hongjian Zhou, Zhipeng Xu, Chun Jiang, Qiuyue Wu, Chuanyue Zhang, Zhenyu Liu, Xiaoxue Zhang, Weiwei Li, Yujia Pang, Jing Zhang and 3 more

Abstract read
In one paragraph

Article in Cell communication and signaling : CCS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors.

Hongjian Zhou *Institute of Laboratory Medicine, Jinling Hospital, First School of Clinical Medicine, Nanjing University School of Medicine, Southern Medical University, Zhongshan East Road 305, Nanjing, Jiangsu, 210002, China.
Zhipeng Xu *Center for Reproductive Medicine and Obstetrics and Gynecology, Nanjing Drum Tower Hospital, Nanjing University Medical School, Nanjing, Jiangsu, 210008, China.
Chun JiangInstitute of Laboratory Medicine, Jinling Hospital, First School of Clinical Medicine, Nanjing University School of Medicine, Southern Medical University, Zhongshan East Road 305, Nanjing, Jiangsu, 210002, China.
Qiuyue WuInstitute of Laboratory Medicine, Jinling Hospital, First School of Clinical Medicine, Nanjing University School of Medicine, Southern Medical University, Zhongshan East Road 305, Nanjing, Jiangsu, 210002, China.
Chuanyue ZhangInstitute of Laboratory Medicine, Jinling Hospital, First School of Clinical Medicine, Nanjing University School of Medicine, Southern Medical University, Zhongshan East Road 305, Nanjing, Jiangsu, 210002, China.
Zhenyu LiuInstitute of Laboratory Medicine, Jinling Hospital, First School of Clinical Medicine, Nanjing University School of Medicine, Southern Medical University, Zhongshan East Road 305, Nanjing, Jiangsu, 210002, China.
Xiaoxue ZhangInstitute of Laboratory Medicine, Jinling Hospital, First School of Clinical Medicine, Nanjing University School of Medicine, Southern Medical University, Zhongshan East Road 305, Nanjing, Jiangsu, 210002, China.
Weiwei LiInstitute of Laboratory Medicine, Jinling Hospital, First School of Clinical Medicine, Nanjing University School of Medicine, Southern Medical University, Zhongshan East Road 305, Nanjing, Jiangsu, 210002, China.
Yujia PangInstitute of Laboratory Medicine, Jinling Hospital, First School of Clinical Medicine, Nanjing University School of Medicine, Southern Medical University, Zhongshan East Road 305, Nanjing, Jiangsu, 210002, China.
Jing ZhangInstitute of Laboratory Medicine, Jinling Hospital, First School of Clinical Medicine, Nanjing University School of Medicine, Southern Medical University, Zhongshan East Road 305, Nanjing, Jiangsu, 210002, China.
Wenju PanInstitute of Laboratory Medicine, Jinling Hospital, First School of Clinical Medicine, Nanjing University School of Medicine, Southern Medical University, Zhongshan East Road 305, Nanjing, Jiangsu, 210002, China.
Min ChenInstitute of Laboratory Medicine, Jinling Hospital, First School of Clinical Medicine, Nanjing University School of Medicine, Southern Medical University, Zhongshan East Road 305, Nanjing, Jiangsu, 210002, China.
Xinyi XiaInstitute of Laboratory Medicine, Jinling Hospital, First School of Clinical Medicine, Nanjing University School of Medicine, Southern Medical University, Zhongshan East Road 305, Nanjing, Jiangsu, 210002, China. xinyixia@nju.edu.cn.

Funding

the Basic Research Plan of Jinling Hospital affiliated to Nanjing University No. 2023JCYJYB103the Basic Research Plan of Jinling Hospital affiliated to Nanjing University No. 2023JCYJYB104the Basic Research Plan of Jinling Hospital affiliated to Nanjing University No. 22JCYYZD9the China Postdoctoral Science Foundation No. 2023M734291
6 · The paper itself

Abstract

introductionIonizing radiation (IR) poses a significant threat to male fertility by inducing substantial changes in the testis, yet the mechanisms underlying IR-induced spermatogenesis disorders remain poorly understood, necessitating the development of more effective radioprotective agents.

methodsWe employed Bulk RNA-seq and single-cell RNA-seq (scRNA-seq) on Balb/c mice testes models following IR exposure to assess cellular and transcriptional alterations. Histological examination, sperm concentration and motility analysis, Western blotting (WB), and reverse transcription quantitative PCR (RT-qPCR) were used to evaluate testicular injury. The therapeutic potential of NF-κB agonists was investigated in an IR-induced spermatogenesis disorder model.

resultsA 6 Gy IR dose induced spermatogenesis disorder and suppressed the spliceosome pathway, predominantly affecting the cell abundance of spermatogonia and primary spermatocytes. Bioinformatics analysis revealed that IR induced splicing disorders in differentiation-related genes, thereby impairing the differentiation ability of primary spermatocytes. Mechanistically, This IR-induced disruption was linked to IR-induced inhibition of NF-κB/Rela and Bclaf1 activity. Notably, NF-κB agonists were found to ameliorate this damage via upregulating Bclaf1 and spliceosome-related genes expression, thereby normalizing splicing patterns and rescuing IR-induced spermatogenesis disorders.

conclusionThis study reveals a novel IR-mediated Rela-Bclaf1-spliceosome regulatory axis in primary spermatocytes and propose Rela as a potential drug target for mitigating IR-induced spermatogenesis disorders. This study not only provides new insights for further research into IR-induced damage and spermatogenic disorders caused by other factors, but also offers potential therapeutic strategies for developing radioprotective agents in cancer radiotherapy.

Indexed as

Radiation, IonizingSpermatocytesSpermatogenesisSpliceosomesTranscription Factor RelAAnimalsMaleMiceMice, Inbred BALB CRela protein, mouseTranscription Factor RelABclaf1Ionizing radiationNF-κB agonistRelascRNA-seqSpermatogenesis dysfunctionSpliceosome

Identifiers

PMID39891142
PMCPMC11786355

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

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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.