Evidence map›Paper›PMID 38212646›Full record

ArticleCell death & disease2024

Low androgen signaling rescues genome integrity with innate immune response by reducing fertility in humans.

J Zimmer, L Mueller, P Frank-Herrmann, J Rehnitz, J E Dietrich, M Bettendorf, T Strowitzki, M Krivega

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.5field-weighted citation impact, top 39% 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

2 citing papers in PubMed, 2 citations in OpenAlex.

  1. Review
  2. Testicular immunity.Molecular aspects of medicine · 2024
    Review
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 at 1 institution in 1 country.

J ZimmerResearch Group of Gonadal Differentiation and Embryonic Development, Department of Gynecological Endocrinology & Fertility Disorders, Women Hospital, University of Heidelberg, 69120, Heidelberg, Germany.
L MuellerResearch Group of Gonadal Differentiation and Embryonic Development, Department of Gynecological Endocrinology & Fertility Disorders, Women Hospital, University of Heidelberg, 69120, Heidelberg, Germany.
P Frank-HerrmannDepartment of Gynecological Endocrinology & Fertility Disorders, Women Hospital, University of Heidelberg, 69120, Heidelberg, Germany.
J RehnitzDepartment of Gynecological Endocrinology & Fertility Disorders, Women Hospital, University of Heidelberg, 69120, Heidelberg, Germany.
J E DietrichDepartment of Gynecological Endocrinology & Fertility Disorders, Women Hospital, University of Heidelberg, 69120, Heidelberg, Germany.ORCID 0000-0003-0022-9502
M BettendorfDivision of Pediatric Endocrinology, Children's Hospital, University of Heidelberg, 69120, Heidelberg, Germany.
T StrowitzkiDepartment of Gynecological Endocrinology & Fertility Disorders, Women Hospital, University of Heidelberg, 69120, Heidelberg, Germany.
M KrivegaResearch Group of Gonadal Differentiation and Embryonic Development, Department of Gynecological Endocrinology & Fertility Disorders, Women Hospital, University of Heidelberg, 69120, Heidelberg, Germany. maria.krivega@med.uni-heidelberg.de.ORCID 0000-0003-1034-8636
Heidelberg University · DE

Funding

University of Heidelberg | Medizinischen Fakultät Heidelberg, Universität Heidelberg (Medical Faculty of Heidelberg, University of Heidelberg) NA
6 · The paper itself

Abstract

Development of the gonads under complex androgen regulation is critical for germ cells specification. In this work we addressed the relationship between androgens and genomic integrity determining human fertility. We used different study groups: individuals with Differences of Sex Development (DSD), including Complete Androgen Insensitivity Syndrome (CAIS) due to mutated androgen receptor (AR), and men with idiopathic nonobstructive azoospermia. Both showed genome integrity status influenced by androgen signaling via innate immune response activation in blood and gonads. Whole proteome analysis connected low AR to interleukin-specific gene expression, while compromised genome stability and tumorigenesis were also supported by interferons. AR expression was associated with predominant DNA damage phenotype, that eliminated AR-positive Sertoli cells as the degeneration of gonads increased. Low AR contributed to resistance from the inhibition of DNA repair in primary leukocytes. Downregulation of androgen promoted apoptosis and specific innate immune response with higher susceptibility in cells carrying genomic instability.

Indexed as

AndrogensReceptors, AndrogenFertilityGonadsHumansImmunity, InnateMaleMutationSertoli CellsAndrogensReceptors, Androgen

Identifiers

PMID38212646
PMCPMC10784536
OpenAlexW4390749073

What OpenQuestion holds

Textmetadata
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.