Evidence map›Paper›PMID 41240254›Full record

ArticleJournal of assisted reproduction and genetics2026

Single-cell analysis of adult mouse testes exposed to cigarette smoke.

Lina Qin, Yun Peng, Nengzhuang Wang, Hongli Yan

Abstract read
In one paragraph

Article in Journal of assisted reproduction and genetics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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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

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

4 authors.

Lina QinReproductive Medicine Center, Changhai Hospital, Naval Medical University, Shanghai, 200433, China.
Yun PengReproductive Medicine Center, Changhai Hospital, Naval Medical University, Shanghai, 200433, China.
Nengzhuang WangReproductive Medicine Center, Changhai Hospital, Naval Medical University, Shanghai, 200433, China.ORCID http://orcid.org/0000-0002-9281-986X
Hongli YanReproductive Medicine Center, Changhai Hospital, Naval Medical University, Shanghai, 200433, China. Hongliyan@smmu.edu.cn.

Funding

Funding for health services Military Medical Research Project BKJ21J007National Key Research and Development Program of Chin 2018YFC1005002National Natural Science Foundation of China 82273465Project of Changhai Hospital 2020YSL009-4Project of Changhai Hospital 2020YXK042Project of Changhai Hospital GH145-36Special Project of Family Planning 20JSZ01
6 · The paper itself

Abstract

backgroundSmoking is a significant global public health concern that has been shown to cause damage to testicular tissue and impair the entire process of spermatogenesis.

methodsA passive smoking mouse model was established to investigate the effects of cigarette smoke exposure. The study included measurements of body weight and testicular weight, pathological assessment of testicular damage, apoptosis experiments, and single-cell RNA sequencing (scRNA-seq) to analyze transcriptomic changes. Additionally, differentially expressed genes were examined, along with gene ontology (GO) analysis and gene set enrichment analysis (GSEA).

resultsBoth testicular weight (control: 126.90 ± 8.26; smoking: 111.60 ± 6.91; P 0.05) and body weight (control: 37.10 ± 1.55; smoking: 27.73 ± 1.20; P 0.0001) were significantly reduced in the smoking group, while the organ coefficient increased significantly (control: 3.31 ± 0.33; smoking: 4.14 ± 0.47; P 0.001). Smoking markedly increased the proportion of apoptotic cells in testicular tissue (control: 0.24 ± 0.08; smoking: 1.06 ± 0.20; P 0.001). ScRNA-seq revealed time-dependent alterations in the proportions of various testicular cell types due to smoking. Smoking affected cytoskeleton and microtubule formation in multiple cell types, as well as flagella development during spermatogenesis. Smoking induced apoptosis across several testicular cell types and disrupted exocrine functions. Mitochondrial energy metabolism was also impaired in multiple cell types. GSEA further supported the induction of apoptosis in various testicular cells.

conclusionSmoking significantly impairs testicular structure and spermatogenesis through multiple mechanisms, including induction of apoptosis, disruption of cellular structure and flagella formation, alteration of exocrine function, and impairment of mitochondrial energy metabolism. These findings highlight the detrimental effects of smoking on male reproductive health at the cellular and molecular levels.

Indexed as

TestisTobacco Smoke PollutionAnimalsApoptosisMaleMiceSingle-Cell AnalysisSmokingSpermatogenesisTranscriptomeTobacco Smoke PollutionAdult mouse testisCigarette smokeSingle-cell RNA sequencingTranscription map

Identifiers

PMID41240254
PMCPMC12831738

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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.