Evidence map›Paper›PMID 41078790›Full record

ArticleACS omega2025

Overactivation of PERK-Mediated Endoplasmic Reticulum Stress-Induced Testis Damage in Chronically Stressed Mice.

Lixuan Peng, Xiaohan Tang, Pingping Tang, Cuilan Zhou, Yuyan Xiang, Wenyu Cao, Yichun Li, Cuiying Peng, Yang Xu, Suyun Li

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in ACS omega, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. The Liver-Testis Axis: Molecular Mechanisms and Clinical Implications.International journal of molecular sciences · 2026
    Review
  2. 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

10 authors.

Lixuan PengClinical Anatomy and Reproductive Medicine Application Institute, Hengyang Medical School, University of South China, Hengyang 421001, Hunan, China.
Xiaohan TangClinical Anatomy and Reproductive Medicine Application Institute, Hengyang Medical School, University of South China, Hengyang 421001, Hunan, China.
Pingping TangClinical Anatomy and Reproductive Medicine Application Institute, Hengyang Medical School, University of South China, Hengyang 421001, Hunan, China.
Cuilan ZhouClinical Anatomy and Reproductive Medicine Application Institute, Hengyang Medical School, University of South China, Hengyang 421001, Hunan, China.
Yuyan XiangClinical Anatomy and Reproductive Medicine Application Institute, Hengyang Medical School, University of South China, Hengyang 421001, Hunan, China.
Wenyu CaoClinical Anatomy and Reproductive Medicine Application Institute, Hengyang Medical School, University of South China, Hengyang 421001, Hunan, China.
Yichun LiDepartment of Obstetrics and Gynecology, The Second Affiliated Hospital, University of South China, Hengyang 421001, Hunan, China.
Cuiying PengDepartment of Cell Biology and Genetics, Hengyang Medical School, University of South China, Hengyang 421001, Hunan, China.
Yang XuInstitute of Neuroscience, Hengyang Medical School, University of South China, Hengyang 421001, Hunan, China.
Suyun LiClinical Anatomy and Reproductive Medicine Application Institute, Hengyang Medical School, University of South China, Hengyang 421001, Hunan, China.ORCID https://orcid.org/0000-0001-8008-3253

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionAlthough endoplasmic reticulum stress (ERS) is known to be associated with spermatogenesis, there is limited information about the role and impact of ERS on chronic stress-induced male infertility.

methodsTo determine the alteration in ERS-related proteins after chronic restraint stress (CRS), these male C57BL/6J mice were randomly divided into the control or CRS group. An ERS inhibitor, integrated stress response inhibitor (ISRIB), was used to establish the causal relationship between ERS and CRS-induced testicular damage, for which male C57BL/6J mice were randomly divided into the following three groups: normal + normal saline (NS), CRS + NS, and CRS + ISRIB. The ERS pathway-related proteins, sperm parameters, testicular structure, spermatogenic cell markers, enzymes involved in steroid biosynthesis, serum corticosterone (CORT) and gonadotropin-releasing hormone (GnRH) levels, and c-fos expression in the hypothalamic paraventricular nucleus (PVN) were evaluated.

resultsCRS primarily activated the pancreatic endoplasmic reticulum kinase (PERK)-mediated ERS pathway in the testis. ISRIB administration improved histology structure, low semen quality, expression of spermatogenic cell markers, and the level of enzymes related to steroid biosynthesis in CRS mice. ISRIB administration also reduced serum CORT levels and normalized hypothalamic PVN neuronal activation, accompanied by increased serum GnRH levels in CRS mice.

conclusionsCRS increased p-PERK expression in the testis. However, treatment with the PERK blocker ISRIB improved sperm quality, preserved testis structure, and rescued the expression of steroidogenesis genes in CRS mice, which might be due to the restoration of the hypothalamic-pituitary-adrenal axis and hypothalamic-pituitary-gonadal function.

Identifiers

PMID41078790
PMCPMC12508973

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.