Evidence map›Paper›PMID 37221631›Full record

ArticleCell & bioscience2023

Identification and validation of CCL2 as a potential biomarker relevant to mast cell infiltration in the testicular immune microenvironment of spermatogenic dysfunction.

Fan Dong, Ping Ping, Si-Qi Wang, Yi Ma, Xiang-Feng Chen

Open access · goldAbstract read
In one paragraph

Article in Cell & bioscience, 2023. 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
3.3field-weighted citation impact, top 8% 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

8 citing papers in PubMed, 12 citations in OpenAlex.

  1. Malignant cell-secreted chemokines drive colorectal cancer progression through endothelial cell activation.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Article
  2. Disulfidptosis-related signatures identify SPARCCellular oncology (Dordrecht, Netherlands) · 2026
    Article
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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

5 authors at 2 institutions in 2 countries.

Fan DongCenter for Reproductive Medicine, School of Medicine, Ren Ji Hospital, Shanghai Jiao Tong University, 845 Lingshan Road, Shanghai, 200135, People's Republic of China.
Ping PingCenter for Reproductive Medicine, School of Medicine, Ren Ji Hospital, Shanghai Jiao Tong University, 845 Lingshan Road, Shanghai, 200135, People's Republic of China.
Si-Qi WangCenter for Reproductive Medicine, School of Medicine, Ren Ji Hospital, Shanghai Jiao Tong University, 845 Lingshan Road, Shanghai, 200135, People's Republic of China.
Yi MaCenter for Reproductive Medicine, School of Medicine, Ren Ji Hospital, Shanghai Jiao Tong University, 845 Lingshan Road, Shanghai, 200135, People's Republic of China. my_july@126.com.
Xiang-Feng ChenCenter for Reproductive Medicine, School of Medicine, Ren Ji Hospital, Shanghai Jiao Tong University, 845 Lingshan Road, Shanghai, 200135, People's Republic of China. allanbacon@163.com.ORCID http://orcid.org/0000-0003-1897-3217
Shanghai Jiao Tong University · CNRenji Hospital · CN

Funding

National Natural Science Foundation of China No.81871199
6 · The paper itself

Abstract

backgroundSpermatogenic dysfunction is an important cause of azoospermia. Numerous studies have focused on germ-cell-related genes that lead to spermatogenic impairment. However, based on the immune-privileged characteristics of the testis, the relationship of immune genes, immune cells or immune microenvironment with spermatogenic dysfunction has rarely been reported.

resultsUsing integrated methods including single-cell RNA-seq, microarray data, clinical data analyses and histological/pathological staining, we found that testicular mast cell infiltration levels were significantly negatively related to spermatogenic function. We next identified a functional testicular immune biomarker, CCL2, and externally validated that testicular CCL2 was significantly upregulated in spermatogenic dysfunctional testes and was negatively correlated with Johnsen scores (JS) and testicular volumes. We also demonstrated that CCL2 levels showed a significant positive correlation with testicular mast cell infiltration levels. Moreover, we showed myoid cells and Leydig cells were two of the important sources of testicular CCL2 in spermatogenic dysfunction. Mechanistically, we drew a potential "myoid/Leydig cells-CCL2-ACKR1-endothelial cells-SELE-CD44-mast cells" network of somatic cell-cell communications in the testicular microenvironment, which might play roles in spermatogenic dysfunction.

conclusionsThe present study revealed CCL2-relevant changes in the testicular immune microenvironment in spermatogenic dysfunction, providing new evidence for the role of immunological factors in azoospermia.

Indexed as

AzoospermiaCCL2Spermatogenic dysfunctionTesticular immune microenvironmentTesticular mast cells

Identifiers

PMID37221631
PMCPMC10204296
OpenAlexW4377939705

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.