Evidence map›Paper›PMID 36537377›Full record

ArticleAsian journal of andrology2023

Exosomes derived from BMSCs ameliorate cyclophosphamide-induced testosterone deficiency by enhancing the autophagy of Leydig cells via the AMPK-mTOR signaling pathway.

Hao-Yu Liang, Fan Peng, Min-Jia Pan, Sen-Lin Liao, Cun Wei, Guan-Yang Wei, Xiao Xie, Kang-Yi Xue, Ming-Kun Chen, Jian-Kun Yang and 3 more

Open access · goldAbstract read
In one paragraph

Article in Asian journal of andrology, 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
0.8field-weighted citation impact, top 30% 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, 10 citations in OpenAlex.

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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

13 authors at 2 institutions in 1 country.

Hao-Yu LiangDepartment of Urology, The Third Affiliated Hospital of Southern Medical University, Guangzhou 510630; The Third School of Clinical Medicine, Southern Medical University, Guangzhou 510515, China.
Fan PengDepartment of Urology, The Third Affiliated Hospital of Southern Medical University, Guangzhou 510630; The Third School of Clinical Medicine, Southern Medical University, Guangzhou 510515, China.
Min-Jia PanThe First School of Clinical Medicine, Southern Medical University, Guangzhou 510515, China.
Sen-Lin LiaoDepartment of Urology, The Third Affiliated Hospital of Southern Medical University, Guangzhou 510630; The Third School of Clinical Medicine, Southern Medical University, Guangzhou 510515, China.
Cun WeiDepartment of Urology, The Third Affiliated Hospital of Southern Medical University, Guangzhou 510630; The Third School of Clinical Medicine, Southern Medical University, Guangzhou 510515, China.
Guan-Yang WeiDepartment of Urology, The Third Affiliated Hospital of Southern Medical University, Guangzhou 510630; The Third School of Clinical Medicine, Southern Medical University, Guangzhou 510515, China.
Xiao XieDepartment of Urology, The Third Affiliated Hospital of Southern Medical University, Guangzhou 510630; The Third School of Clinical Medicine, Southern Medical University, Guangzhou 510515, China.
Kang-Yi XueDepartment of Urology, The Third Affiliated Hospital of Southern Medical University, Guangzhou 510630; The Third School of Clinical Medicine, Southern Medical University, Guangzhou 510515, China.
Ming-Kun ChenDepartment of Urology, The Third Affiliated Hospital of Southern Medical University, Guangzhou 510630; The Third School of Clinical Medicine, Southern Medical University, Guangzhou 510515, China.
Jian-Kun YangDepartment of Urology, The Third Affiliated Hospital of Southern Medical University, Guangzhou 510630; The Third School of Clinical Medicine, Southern Medical University, Guangzhou 510515, China.
Wen-Bin GuoDepartment of Urology, The Third Affiliated Hospital of Southern Medical University, Guangzhou 510630; The Third School of Clinical Medicine, Southern Medical University, Guangzhou 510515, China.
Cun-Dong LiuDepartment of Urology, The Third Affiliated Hospital of Southern Medical University, Guangzhou 510630; The Third School of Clinical Medicine, Southern Medical University, Guangzhou 510515, China.
Qi-Zhao ZhouDepartment of Urology, The Third Affiliated Hospital of Southern Medical University, Guangzhou 510630; The Third School of Clinical Medicine, Southern Medical University, Guangzhou 510515, China.
Third Affiliated Hospital of Southern Medical University · CNSouthern Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cyclophosphamide-induced testosterone deficiency (CPTD) during the treatment of cancers and autoimmune disorders severely influences the quality of life of patients. Currently, several guidelines recommend patients suffering from CPTD receive testosterone replacement therapy (TRT). However, TRT has many disadvantages underscoring the requirement for alternative, nontoxic treatment strategies. We previously reported bone marrow mesenchymal stem cells-derived exosomes (BMSCs-exos) could alleviate cyclophosphamide (CP)-induced spermatogenesis dysfunction, highlighting their role in the treatment of male reproductive disorders. Therefore, we further investigated whether BMSCs-exos affect autophagy and testosterone synthesis in Leydig cells (LCs). Here, we examined the effects and probed the molecular mechanisms of BMSCs-exos on CPTD in vivo and in vitro by detecting the expression levels of genes and proteins related to autophagy and testosterone synthesis. Furthermore, the testosterone concentration in serum and cell-conditioned medium, and the photophosphorylation protein levels of adenosine monophosphate-activated protein kinase (AMPK) and mammalian target of rapamycin (mTOR) were measured. Our results suggest that BMSCs-exos could be absorbed by LCs through the blood-testis barrier in mice, promoting autophagy in LCs and improving the CP-induced low serum testosterone levels. BMSCs-exos inhibited cell death in CP-exposed LCs, regulated the AMPK-mTOR signaling pathway to promote autophagy in LCs, and then improved the low testosterone synthesis ability of CP-induced LCs. Moreover, the autophagy inhibitor, 3-methyladenine (3-MA), significantly reversed the therapeutic effects of BMSCs-exos. These findings suggest that BMSCs-exos promote LC autophagy by regulating the AMPK-mTOR signaling pathway, thereby ameliorating CPTD. This study provides novel evidence for the clinical improvement of CPTD using BMSCs-exos.

Indexed as

AMP-Activated Protein KinasesExosomesAnimalsAutophagyLeydig CellsMaleMammalsMiceQuality of LifeSignal TransductionTestosteroneTOR Serine-Threonine KinasesAMP-Activated Protein KinasesTestosteroneTOR Serine-Threonine Kinasesautophagybone marrow mesenchymal stem cellscyclophosphamideexosomesLeydig cellstestosterone deficiency

Identifiers

PMID36537377
PMCPMC10411264
OpenAlexW4312018525

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.