Evidence map›Paper›PMID 42174225›Full record

ArticleHistochemistry and cell biology2026

A rapid and robust translational model for testicular aging research.

N Schmid, Y Stepanov, M Offner, L Scholz, C Herrmann, S Petkov, R Behr, J B Stöckl, T Fröhlich, A Mayerhofer

Abstract read
In one paragraph

Article in Histochemistry and cell biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. June in focus in HCB: advanced methodologies.Histochemistry and cell biology · 2026
    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

10 authors.

N SchmidBiomedical Center (BMC), Cell Biology, Anatomy III, Faculty of Medicine, Ludwig Maximilian University Munich (LMU), 82152, Planegg, Germany.
Y StepanovLaboratory for Functional Genome Analysis LAFUGA, Gene Center, Ludwig Maximilian University of Munich (LMU), 81377, Munich, Germany.
M OffnerBiomedical Center (BMC), Cell Biology, Anatomy III, Faculty of Medicine, Ludwig Maximilian University Munich (LMU), 82152, Planegg, Germany.
L ScholzBiomedical Center (BMC), Cell Biology, Anatomy III, Faculty of Medicine, Ludwig Maximilian University Munich (LMU), 82152, Planegg, Germany.
C HerrmannBiomedical Center (BMC), Cell Biology, Anatomy III, Faculty of Medicine, Ludwig Maximilian University Munich (LMU), 82152, Planegg, Germany.
S PetkovStammzell- und Regenerationsbiologie, German Primate Center, Leibniz Institute for Primate Research, 37077, Göttingen, Germany.
R BehrStammzell- und Regenerationsbiologie, German Primate Center, Leibniz Institute for Primate Research, 37077, Göttingen, Germany.
J B StöcklLaboratory for Functional Genome Analysis LAFUGA, Gene Center, Ludwig Maximilian University of Munich (LMU), 81377, Munich, Germany.
T FröhlichLaboratory for Functional Genome Analysis LAFUGA, Gene Center, Ludwig Maximilian University of Munich (LMU), 81377, Munich, Germany.
A MayerhoferBiomedical Center (BMC), Cell Biology, Anatomy III, Faculty of Medicine, Ludwig Maximilian University Munich (LMU), 82152, Planegg, Germany. mayerhofer@bmc.med.lmu.de.ORCID http://orcid.org/0000-0002-9388-4639

Funding

Deutsche Forschungsgeme #491030536 and #427588170
6 · The paper itself

Abstract

In humans, testicular peritubular cells (TPCs) form a small compartment surrounding the seminiferous tubules and, as shown previously, undergo age-related changes. How they may contribute to the age-associated decline of testicular functions is not well known. Likewise, the mechanisms of testicular aging in humans are not well examined. This is in part due to the lack of appropriate cellular models. We aimed to establish an aging model of TPCs, which is based on immortalized nonhuman primate (NHP) peritubular cells (iMKTPCs) from Callithrix jacchus. As shown previously by a comprehensive proteomic approach, they strongly resemble human TPCs but lack the human cell-intrinsic heterogeneity. Cellular senescence was robustly induced within 10 days upon exposure to 25 µg/mL bleomycin for 24 h. This resulted in increased β-galactosidase activity, enlarged cells, and elevated transcript levels of senescence-associated secretory phenotype (SASP) molecules (IL1b, TNFa, CCL2). The ability to contract upon a stimulus was reduced, as shown in live cell imaging studies. Reduced proliferation among others was indicated by a decreased abundance of proliferating cell nuclear antigen (PCNA), evident in a proteomic analysis, which also revealed massive changes (341 significantly increased and 372 decreased proteins). Bioinformatics analysis indicated a marked reduction in several cell-motility-associated proteins, whereas proteins linked to extracellular exosomes, the cytoskeleton, and lysosomal pathways were increased in abundance. To conclude, bleomycin treatment causes a rapid and robust induction of cellular senescence in a translational testicular cell model of peritubular cells. This model will enable future studies aiming to explore mechanisms and consequences of testicular aging.

Indexed as

AgingCellular SenescenceTestisTranslational Research, BiomedicalAnimalsBleomycinCells, CulturedHumansMaleProteomicsBleomycinPeritubular cellsSenescenceTestisTranslational model

Identifiers

PMID42174225
PMCPMC13197275

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.