Evidence map›Paper›PMID 40728777›Full record

ArticleCurrent medical science2025

Chop Deficiency Exacerbates Cyclophosphamide-Induced Overactive Bladder via Impaired Macrophage Apoptosis.

Ya-Nan Wang, Xiang-Dong Guo, Chun-Yu Zhang, Bi-Ying Wang, Jun Xiao, Xue-You Ma, Shu Zhang, Zhi-Quan Hu, Xiao-Yi Yuan, Zhi-Hua Wang and 1 more

Abstract read
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Article in Current medical science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

11 authors.

Ya-Nan WangDepartment of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
Xiang-Dong GuoDepartment of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
Chun-Yu ZhangDepartment of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
Bi-Ying WangDepartment of Urology, Wuxue First People's Hospital, Wuxue, 435400, China.
Jun XiaoDepartment of Thyroid and Breast Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
Xue-You MaDepartment of Urology, the First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, 310003, China.
Shu ZhangThe Center for Biomedical Research, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
Zhi-Quan HuDepartment of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
Xiao-Yi YuanDepartment of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
Zhi-Hua WangDepartment of Urology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.ORCID http://orcid.org/0000-0002-5155-1457
Wei KeDepartment of Urology, Wuxue First People's Hospital, Wuxue, 435400, China. 34439095@qq.com.

Funding

National Natural Science Foundation of China 82173068National Natural Science Foundation of China Nos. 81974400
6 · The paper itself

Abstract

objectiveOveractive bladder, a storage syndrome characterized by urinary urgency, frequency, and nocturia with or without urgency urinary incontinence, severely affects the quality of life of patients. The aim of this study was to investigate the role and mechanism of the C/EBP homologous protein in the overactive bladder.

methodsAn overactive bladder mouse model was established via the intraperitoneal injection of cyclophosphamide in wild-type and Chop-deficient mice. An in vitro model was established using interleukin (IL)-6-induced mouse bladder epithelial cells. Hematoxylin-eosin (HE) staining was used to assess bladder tissue damage, and ELISA was used to measure inflammatory cytokine levels. Western blot analysis was used to examine p-PERK, ATF-6, p-eIF2α, BiP, ATF-4, Bax, Bcl-2, and cleaved caspase-3 protein expression levels. TUNEL staining and flow cytometry were conducted to measure the degree of apoptosis in bladder epithelial cells and macrophages.

resultsC/EBP homologous protein levels were decreased in overactive bladder tissues; nevertheless, macrophage infiltration was found to be increased. Knockout of Chop exacerbated bladder dysfunction, tissue injury, macrophage infiltration, and bladder epithelial apoptosis and alleviated endoplasmic reticulum stress.

conclusionsChop deficiency exacerbates inflammation, injury, and bladder epithelial apoptosis in overactive bladder model mice by inhibiting endoplasmic reticulum stress.

Indexed as

ApoptosisCyclophosphamideMacrophagesTranscription Factor CHOPUrinary Bladder, OveractiveAnimalsDisease Models, AnimalEndoplasmic Reticulum StressEpithelial CellsInterleukin-6MaleMiceMice, KnockoutUrinary BladderCyclophosphamideDdit3 protein, mouseInterleukin-6Transcription Factor CHOPApoptosisC/EBP homologous proteinCyclophosphamideEndoplasmic reticulum stressInflammationMacrophageOveractive bladder

Identifiers

PMID40728777

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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.