Evidence map›Paper›PMID 37993934›Full record

ArticleBMC medicine2023

Epididymal RNase T2 contributes to astheno-teratozoospermia and intergenerational metabolic disorder through epididymosome-sperm interaction.

Zhuoyao Ma, Jinyu Li, Li Fu, Rong Fu, Ningyuan Tang, Yanmei Quan, Zhixiang Xin, Zhide Ding, Yue Liu

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in BMC medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
4.6field-weighted citation impact, top 5% of its field
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

16 citing papers in PubMed, 17 citations in OpenAlex.

  1. Review
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  8. Environmental and Genetic Perturbations of the Sperm Epigenome.Advances in experimental medicine and biology · 2026
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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

9 authors at 2 institutions in 1 country.

Zhuoyao Ma *Department of Histology, Embryology, Genetics and Developmental Biology, Shanghai Key Laboratory for Reproductive Medicine, Shanghai Jiao Tong University School of Medicine, No.280, Chongqing Road (South), Shanghai, 200025, China.
Jinyu Li *Department of Histology, Embryology, Genetics and Developmental Biology, Shanghai Key Laboratory for Reproductive Medicine, Shanghai Jiao Tong University School of Medicine, No.280, Chongqing Road (South), Shanghai, 200025, China.
Li Fu *Department of Laboratory Animal Science, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China.
Rong FuCore Facility of Basic Medical Sciences, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China.
Ningyuan TangDepartment of Histology, Embryology, Genetics and Developmental Biology, Shanghai Key Laboratory for Reproductive Medicine, Shanghai Jiao Tong University School of Medicine, No.280, Chongqing Road (South), Shanghai, 200025, China.
Yanmei QuanDepartment of Histology, Embryology, Genetics and Developmental Biology, Shanghai Key Laboratory for Reproductive Medicine, Shanghai Jiao Tong University School of Medicine, No.280, Chongqing Road (South), Shanghai, 200025, China.
Zhixiang XinDepartment of Urology, Shanghai Changzheng Hospital, Naval Medical University, No. 415, Fengyang Road, Shanghai, 200003, China. xiaoxin973@hotmail.com.ORCID 0009-0007-7502-5762
Zhide DingDepartment of Histology, Embryology, Genetics and Developmental Biology, Shanghai Key Laboratory for Reproductive Medicine, Shanghai Jiao Tong University School of Medicine, No.280, Chongqing Road (South), Shanghai, 200025, China. 1545418815@qq.com.
Yue LiuDepartment of Histology, Embryology, Genetics and Developmental Biology, Shanghai Key Laboratory for Reproductive Medicine, Shanghai Jiao Tong University School of Medicine, No.280, Chongqing Road (South), Shanghai, 200025, China. liuyue@shsmu.edu.cn.ORCID 0000-0002-2700-922X
Shanghai Jiao Tong University · CNShanghai Changzheng Hospital · CN

Funding

National Natural Science Foundation of China 81701503National Natural Science Foundation of China 81971437National Natural Science Foundation of China 82071694National Natural Science Foundation of China 82171595Science and Technology Innovation Plan Of Shanghai Science and Technology Commission 201409005800Science and Technology Innovation Plan Of Shanghai Science and Technology Commission 21140904000Science and Technology Innovation Plan Of Shanghai Science and Technology Commission 22140904200Science and Technology Innovation Plan Of Shanghai Science and Technology Commission 23ZR1436000
6 · The paper itself

Abstract

backgroundThe epididymis is crucial for post-testicular sperm development which is termed sperm maturation. During this process, fertilizing ability is acquired through the epididymis-sperm communication via exchange of protein and small non-coding RNAs (sncRNAs). More importantly, epididymal-derived exosomes secreted by the epididymal epithelial cells transfer sncRNAs into maturing sperm. These sncRNAs could mediate intergenerational inheritance which further influences the health of their offspring. Recently, the linkage and mechanism involved in regulating sperm function and sncRNAs during epididymal sperm maturation are increasingly gaining more and more attention.

methodsAn epididymal-specific ribonuclease T2 (RNase T2) knock-in (KI) mouse model was constructed to investigate its role in developing sperm fertilizing capability. The sperm parameters of RNase T2 KI males were evaluated and the metabolic phenotypes of their offspring were characterized. Pandora sequencing technology profiled and sequenced the sperm sncRNA expression pattern to determine the effect of epididymal RNase T2 on the expression levels of sperm sncRNAs. Furthermore, the expression levels of RNase T2 in the epididymal epithelial cells in response to environmental stress were confirmed both in vitro and in vivo.

resultsOverexpression of RNase T2 caused severe subfertility associated with astheno-teratozoospermia in mice caput epididymis, and furthermore contributed to the acquired metabolic disorders in the offspring, including hyperglycemia, hyperlipidemia, and hyperinsulinemia. Pandora sequencing showed altered profiles of sncRNAs especially rRNA-derived small RNAs (rsRNAs) and tRNA-derived small RNAs (tsRNAs) in RNase T2 KI sperm compared to control sperm. Moreover, environmental stress upregulated RNase T2 in the caput epididymis.

conclusionsThe importance was demonstrated of epididymal RNase T2 in inducing sperm maturation and intergenerational inheritance. Overexpressed RNase T2 in the caput epididymis leads to astheno-teratozoospermia and metabolic disorder in the offspring.

Indexed as

Metabolic DiseasesRNA, Small UntranslatedAnimalsEndoribonucleasesEpididymisMaleMiceSemenSpermatozoaEndoribonucleasesribonuclease T(2)RNA, Small UntranslatedAstheno-teratozoospermiaIntergenerational metabolic inheritanceRibonuclease T2Small non-coding RNAsSperm maturation

Identifiers

PMID37993934
PMCPMC10664275
OpenAlexW4388904896

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.