Evidence map›Paper›PMID 34894202›Full record

ArticleJournal of cellular and molecular medicine2022

Chronic stress inhibits testosterone synthesis in Leydig cells through mitochondrial damage via Atp5a1.

Xiaofan Xiong, Qiuhua Wu, Lingyu Zhang, Shanfeng Gao, Rufeng Li, Lin Han, Meiyang Fan, Miaomiao Wang, Liying Liu, Xiaofei Wang and 5 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.6field-weighted citation impact, top 9% 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

12 citing papers in PubMed, 27 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors at 3 institutions in 1 country.

Xiaofan XiongWestern China Science and Technology Innovation Port in Precision Medicine Institute, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.ORCID 0000-0001-8793-2713
Qiuhua WuKey Laboratory of Environment and Genes Related to Diseases, Ministry of Education of China, Xi'an Jiaotong University, Xi'an, China.
Lingyu ZhangDepartment of Cell Biology and Genetics, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, Xi'an, China.
Shanfeng GaoDepartment of Cell Biology and Genetics, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, Xi'an, China.
Rufeng LiDepartment of Cell Biology and Genetics, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, Xi'an, China.
Lin HanKey Laboratory of Environment and Genes Related to Diseases, Ministry of Education of China, Xi'an Jiaotong University, Xi'an, China.
Meiyang FanDepartment of Cell Biology and Genetics, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, Xi'an, China.
Miaomiao WangDepartment of Cell Biology and Genetics, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, Xi'an, China.
Liying LiuKey Laboratory of Environment and Genes Related to Diseases, Ministry of Education of China, Xi'an Jiaotong University, Xi'an, China.
Xiaofei WangKey Laboratory of Environment and Genes Related to Diseases, Ministry of Education of China, Xi'an Jiaotong University, Xi'an, China.
Chunli ZhangWestern China Science and Technology Innovation Port in Precision Medicine Institute, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
Yanlong XinWestern China Science and Technology Innovation Port in Precision Medicine Institute, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
Zongfang LiWestern China Science and Technology Innovation Port in Precision Medicine Institute, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
Chen HuangDepartment of Cell Biology and Genetics, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, Xi'an, China.
Juan YangDepartment of Cell Biology and Genetics, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, Xi'an, China.
Xi'an Jiaotong University · CNSecond Affiliated Hospital of Xi'an Jiaotong University · CNNorthwest Women's and Children's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Stress is one of the leading causes of male infertility, but its exact function in testosterone synthesis has scarcely been reported. We found that adult male rats show a decrease in bodyweight, genital index and serum testosterone level after continual chronic stress for 21 days. Two-dimensional gel electrophoresis (2-DE) and MALDI-TOF-MS analysis identified 10 differentially expressed proteins in stressed rats compared with controls. A strong protein interaction network was found to be centred on Atp5a1 among these proteins. Atp5a1 expression significantly decreased in Leydig cells after chronic stress. Transfection of Atp5a1 siRNAs decreased StAR, CYP11A1, and 17β-HSD expression by damaging the structure of mitochondria in TM3 cells. This study confirmed that chronic stress plays an important role in testosterone synthesis by regulating Atp5a1 expression in Leydig cells.

Indexed as

Leydig CellsTestosteroneAnimalsCholesterol Side-Chain Cleavage EnzymeMaleMitochondriaMitochondrial Proton-Translocating ATPasesRatsCholesterol Side-Chain Cleavage EnzymeMitochondrial Proton-Translocating ATPasesTestosteroneAtp5a1Leydig cellsmitochondrial dysfunctiontestosterone synthesis

Identifiers

PMID34894202
PMCPMC8743653
OpenAlexW4200307676

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.