Evidence map›Paper›PMID 35111154›Full record

ArticleFrontiers in immunology2021

High Throughput scRNA-Seq Provides Insights Into Leydig Cell Senescence Induced by Experimental Autoimmune Orchitis: A Prominent Role of Interstitial Fibrosis and Complement Activation.

Yinchuan Li, Panpan Mi, Jiabao Wu, Yunge Tang, Xiaohua Liu, Jinmei Cheng, Yingying Huang, Weibing Qin, C Yan Cheng, Fei Sun

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
8.5field-weighted citation impact, top 2% 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

16 citing papers in PubMed, 46 citations in OpenAlex.

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  12. Functional genomics in Spiralia.Briefings in functional genomics · 2023
    Article
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  16. Testis-enrichedAmerican journal of translational research · 2022
    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 at 2 institutions in 2 countries.

Yinchuan LiInstitute of Reproductive Medicine, Medical School of Nantong University, Nantong, China.
Panpan MiInstitute of Reproductive Medicine, Medical School of Nantong University, Nantong, China.
Jiabao WuNHC Key Laboratory of Male Reproduction and Genetics, Guangdong Provincial Reproductive Science Institute (Guangdong Provincial Fertility Hospital), Guangzhou, China.
Yunge TangNHC Key Laboratory of Male Reproduction and Genetics, Guangdong Provincial Reproductive Science Institute (Guangdong Provincial Fertility Hospital), Guangzhou, China.
Xiaohua LiuNHC Key Laboratory of Male Reproduction and Genetics, Guangdong Provincial Reproductive Science Institute (Guangdong Provincial Fertility Hospital), Guangzhou, China.
Jinmei ChengInstitute of Reproductive Medicine, Medical School of Nantong University, Nantong, China.
Yingying HuangInstitute of Reproductive Medicine, Medical School of Nantong University, Nantong, China.
Weibing QinNHC Key Laboratory of Male Reproduction and Genetics, Guangdong Provincial Reproductive Science Institute (Guangdong Provincial Fertility Hospital), Guangzhou, China.
C Yan ChengThe Mary M. Wohlford Laboratory for Male Contraceptive Research, Center for Biomedical Research, Population Council, New York, NY, United States.
Fei SunInstitute of Reproductive Medicine, Medical School of Nantong University, Nantong, China.
Nantong University · CNPopulation Council · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Leydig cells (Lc), located in the interstitial space of the testis between seminiferous tubules, produce 95% of testosterone in male individuals, which is pivotal for male sexual differentiation, spermatogenesis, and maintenance of the male secondary sex characteristics. Lc are prone to senescence in aging testes, resulting in compromised androgen synthesis capability upon aging. However, little is known about whether Lc undergo senescence in a chronic inflammatory environment. To investigate this question, mouse models of experimental autoimmune orchitis (EAO) were used, and Lc were analyzed by high throughput scRNA-Seq. Data were screened and analyzed by correlating signaling pathways with senescence, apoptosis, androgen synthesis, and cytokine/chemokine signaling pathways. EAO did induce Lc senescence, and Lc senescence in turn antagonized androgen synthesis. Based on the correlation screening of pathways inducing Lc senescence, a plethora of pathways were found to play potential roles in triggering Lc senescence during EAO, among which the

Indexed as

AngiopoietinsAnimalsApoptosisAutoimmune DiseasesCellular SenescenceComplement ActivationCytokinesDisease Models, AnimalFibrosisLeydig CellsMaleMiceMice, Inbred C57BLSignal TransductionSingle-Cell AnalysisAngiopoietinsCytokinesandrogen synthesiscomplementcytokinesexperimental autoimmune orchitis (EAO)fibrosisglutathione metabolismLeydig cellsscRNA-Seq

Identifiers

PMID35111154
PMCPMC8801941
OpenAlexW4206723224

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.