Evidence map›Paper›PMID 39283662›Full record

ArticleeLife2024

Mechanistic target of rapamycin (mTOR) pathway in Sertoli cells regulates age-dependent changes in sperm DNA methylation.

Saira Amir, Olatunbosun Arowolo, Ekaterina Mironova, Joseph McGaunn, Oladele Oluwayiose, Oleg Sergeyev, J Richard Pilsner, Alexander Suvorov

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in eLife, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing 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

8 citing papers in PubMed.

  1. Trial
  2. Article
  3. Advances in immunological research on male infertility.Frontiers in reproductive health · 2026
    Review
  4. Article
  5. Review
  6. Article
  7. Testicular immunity.Molecular aspects of medicine · 2024
    Review
  8. 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

8 authors.

Saira Amir *Department of Environmental Health Sciences, University of Massachusetts, Amherst, United States.ORCID https://orcid.org/0000-0002-1864-8572
Olatunbosun Arowolo *Department of Environmental Health Sciences, University of Massachusetts, Amherst, United States.
Ekaterina MironovaBelozersky Institute of Physico-Chemical Biology, Lomonosov Moscow State University, Moscow, Russian Federation.
Joseph McGaunnDepartment of Environmental Health Sciences, University of Massachusetts, Amherst, United States.
Oladele OluwayioseDepartment of Obstetrics and Gynecology, Wayne State University, Detroit, United States.
Oleg SergeyevBelozersky Institute of Physico-Chemical Biology, Lomonosov Moscow State University, Moscow, Russian Federation.
J Richard PilsnerDepartment of Obstetrics and Gynecology, Wayne State University, Detroit, United States.
Alexander SuvorovDepartment of Environmental Health Sciences, University of Massachusetts, Amherst, United States.ORCID https://orcid.org/0000-0002-2757-5897

Funding

School of Public Health and Health Sciences, University of Massachusetts Amherst Dean's Research Enhancement Award
6 · The paper itself

Abstract

Over the past several decades, a trend toward delayed childbirth has led to increases in parental age at the time of conception. Sperm epigenome undergoes age-dependent changes increasing risks of adverse conditions in offspring conceived by fathers of advanced age. The mechanism(s) linking paternal age with epigenetic changes in sperm remain unknown. The sperm epigenome is shaped in a compartment protected by the blood-testes barrier (BTB) known to deteriorate with age. Permeability of the BTB is regulated by the balance of two mTOR complexes in Sertoli cells where mTOR complex 1 (mTORC1) promotes the opening of the BTB and mTOR complex 2 (mTORC2) promotes its integrity. We hypothesized that this balance is also responsible for age-dependent changes in the sperm epigenome. To test this hypothesis, we analyzed reproductive outcomes, including sperm DNA methylation in transgenic mice with Sertoli cell-specific suppression of mTORC1 (

Indexed as

DNA MethylationSertoli CellsSpermatozoaAgingAnimalsEpigenesis, GeneticMaleMechanistic Target of Rapamycin Complex 1Mechanistic Target of Rapamycin Complex 2MiceMice, KnockoutMice, TransgenicRapamycin-Insensitive Companion of mTOR ProteinRegulatory-Associated Protein of mTORSignal TransductionTOR Serine-Threonine KinasesMechanistic Target of Rapamycin Complex 1Mechanistic Target of Rapamycin Complex 2mTOR protein, mouseRapamycin-Insensitive Companion of mTOR ProteinRegulatory-Associated Protein of mTORrictor protein, mouseRptor protein, mouseTOR Serine-Threonine Kinasesagingdevelopmental biologyDNA methylationepigeneticmousemTORrejuvenationsperm

Identifiers

PMID39283662
PMCPMC11405012

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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.