Evidence map›Paper›PMID 38846492›Full record

ReviewFrontiers in endocrinology2024

Research progress on the fanconi anemia signaling pathway in non-obstructive azoospermia.

Haohui Xu, Yixin Zhang, Caiqin Wang, Zhuoyan Fu, Jing Lv, Yufang Yang, Zihan Zhang, Yuanmin Qi, Kai Meng, Jinxiang Yuan and 1 more

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Frontiers in endocrinology, 2024. 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. 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

11 authors.

Haohui Xu *Lin He's Academician Workstation of New Medicine and Clinical Translation, Jining Medical University, Jining, China.
Yixin Zhang *Lin He's Academician Workstation of New Medicine and Clinical Translation, Jining Medical University, Jining, China.
Caiqin Wang *Lin He's Academician Workstation of New Medicine and Clinical Translation, Jining Medical University, Jining, China.
Zhuoyan FuLin He's Academician Workstation of New Medicine and Clinical Translation, Jining Medical University, Jining, China.
Jing LvLin He's Academician Workstation of New Medicine and Clinical Translation, Jining Medical University, Jining, China.
Yufang YangLin He's Academician Workstation of New Medicine and Clinical Translation, Jining Medical University, Jining, China.
Zihan ZhangLin He's Academician Workstation of New Medicine and Clinical Translation, Jining Medical University, Jining, China.
Yuanmin QiLin He's Academician Workstation of New Medicine and Clinical Translation, Jining Medical University, Jining, China.
Kai MengLin He's Academician Workstation of New Medicine and Clinical Translation, Jining Medical University, Jining, China.
Jinxiang YuanLin He's Academician Workstation of New Medicine and Clinical Translation, Jining Medical University, Jining, China.
Xiaomei WangCollege of Basic Medicine, Jining Medical University, Jining, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Non-obstructive azoospermia (NOA) is a disease characterized by spermatogenesis failure and comprises phenotypes such as hypospermatogenesis, mature arrest, and Sertoli cell-only syndrome. Studies have shown that FA cross-linked anemia (FA) pathway is closely related to the occurrence of NOA. There are FA gene mutations in male NOA patients, which cause significant damage to male germ cells. The FA pathway is activated in the presence of DNA interstrand cross-links; the key step in activating this pathway is the mono-ubiquitination of the FANCD2-FANCI complex, and the activation of the FA pathway can repair DNA damage such as DNA double-strand breaks. Therefore, we believe that the FA pathway affects germ cells during DNA damage repair, resulting in minimal or even disappearance of mature sperm in males. This review summarizes the regulatory mechanisms of FA-related genes in male azoospermia, with the aim of providing a theoretical reference for clinical research and exploration of related genes.

Indexed as

AzoospermiaFanconi Anemia Complementation Group ProteinsSignal TransductionAnimalsDNA DamageDNA RepairHumansMaleSpermatogenesisFanconi Anemia Complementation Group ProteinsFanconi anemia geneFanconi anemia pathwayhomologous recombinationinterstrand crosslinksnon-obstructive azoospermia

Identifiers

PMID38846492
PMCPMC11153779

What OpenQuestion holds

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Registered trials

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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.