Evidence map›Paper›PMID 40442779›Full record

ArticleMilitary Medical Research2025

Salmonella enterica mediated epigenetic promotion of fibrosis is a novel factor in benign prostatic hyperplasia.

Cong Zhu, Lu-Yao Li, Ming-Hui Shi, Cheng Fang, Lu Yang, Ting Li, Fei Li, Shi-Song Yang, Tian-Kun Wang, Dao-Jing Ming and 9 more

Abstract read
In one paragraph

Article in Military Medical Research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 1 pooled it
–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

6 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Review
  6. 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

19 authors.

Cong Zhu *Center for Evidence-Based and Translational Medicine, Zhongnan Hospital of Wuhan University, Wuhan, 430071, China.
Lu-Yao Li *Center for Evidence-Based and Translational Medicine, Zhongnan Hospital of Wuhan University, Wuhan, 430071, China.
Ming-Hui Shi *Center for Evidence-Based and Translational Medicine, Zhongnan Hospital of Wuhan University, Wuhan, 430071, China.
Cheng FangCenter for Evidence-Based and Translational Medicine, Zhongnan Hospital of Wuhan University, Wuhan, 430071, China.
Lu YangDepartment of Urology, West China Hospital, Sichuan University, Chengdu, 610041, China.
Ting LiCenter for Evidence-Based and Translational Medicine, Zhongnan Hospital of Wuhan University, Wuhan, 430071, China.
Fei LiCenter for Evidence-Based and Translational Medicine, Zhongnan Hospital of Wuhan University, Wuhan, 430071, China.
Shi-Song YangCenter for Evidence-Based and Translational Medicine, Zhongnan Hospital of Wuhan University, Wuhan, 430071, China.
Tian-Kun WangCenter for Evidence-Based and Translational Medicine, Zhongnan Hospital of Wuhan University, Wuhan, 430071, China.
Dao-Jing MingCenter for Evidence-Based and Translational Medicine, Zhongnan Hospital of Wuhan University, Wuhan, 430071, China.
Tong DengCenter for Evidence-Based and Translational Medicine, Zhongnan Hospital of Wuhan University, Wuhan, 430071, China.
Hao-Yue SunCenter for Evidence-Based and Translational Medicine, Zhongnan Hospital of Wuhan University, Wuhan, 430071, China.
Wen-Ting LiCenter for Evidence-Based and Translational Medicine, Zhongnan Hospital of Wuhan University, Wuhan, 430071, China.
Jia ZhangCenter for Evidence-Based and Translational Medicine, Zhongnan Hospital of Wuhan University, Wuhan, 430071, China.
Yu-Sen ZhangCenter for Evidence-Based and Translational Medicine, Zhongnan Hospital of Wuhan University, Wuhan, 430071, China.
Zhi-Yuan JianDepartment of Gastrointestinal Surgery, the First Affiliated Hospital of Guilin Medical University, Guilin, 541001, Guangxi, China. jianzhiyuan2001@163.com.
Chang-Jiang QinDepartment of Gastrointestinal Surgery, Huaihe Hospital of Henan University, Kaifeng, 475000, Henan, China. hhyyqcj@vip.henu.edu.cn.
Shuang-Ying WangCenter for Evidence-Based and Translational Medicine, Zhongnan Hospital of Wuhan University, Wuhan, 430071, China. wangshuangying@whu.edu.cn.
Xian-Tao ZengCenter for Evidence-Based and Translational Medicine, Zhongnan Hospital of Wuhan University, Wuhan, 430071, China. zengxiantao1128@whu.edu.cn.ORCID 0000-0003-1262-725X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundFibrosis constitutes a significant pathophysiological mechanism in the clinical progression of benign prostatic hyperplasia (BPH) and represents a contributing factor to the ineffectiveness of prevailing pharmacological treatments. Emerging evidence suggests a close association between microbial presence and the development of fibrosis. Nonetheless, the potential involvement of microbes within prostatic tissue in the pathogenesis of BPH and prostatic fibrosis, along with the underlying mechanisms, remains unexplored.

methodsUtilizing immunohistochemistry and microbial sequencing, we analyzed the microbes of prostate tissues from BPH patients with different degrees of prostate fibrosis and found that Salmonella enterica (S. enterica) was enriched in the high degree of prostate fibrosis. We developed prostate cell and animal models infected with the lipopolysaccharide of S. enterica (S.e-LPS) to assess its impact on prostate fibrosis. To elucidate the underlying functional mechanisms, we employed molecular biology techniques, including RNA degradation assays, N

resultsMicrobial diversity differed between low- and high-fibrosis groups, with S. enterica showing the highest mean abundance among the four species that differed significantly. S.e-LPS was detected in S. enterica-rich prostate tissue and was found to significantly promote cell proliferation, cell contractility, lipid peroxidation, and the induction of ferroptosis. Animal experiments demonstrated that S.e-LPS infection led to pronounced hyperplasia of the prostatic epithelium, with epithelial thickness increasing to 1.57 times that of the sham group, and collagen fibrosis increasing to 2.84 times that of the sham group, thereby exacerbating prostatic tissue fibrosis in rats. In vitro experiments further revealed that S.e-LPS promoted prostate cell fibrosis by inducing ferroptosis. Mechanistically, it was determined that S.e-LPS regulates ferroptosis via AlkB homolog 5 (ALKBH5)-mediated m

conclusionThe findings of this study suggest that S. enterica promotes prostatic fibrosis through ALKBH5-m

Indexed as

Epigenesis, GeneticFibrosisProstatic HyperplasiaSalmonella entericaAgedAnimalsDisease Models, AnimalHumansMaleProstateAlkB homolog 5 (ALKBH5)Benign prostatic hyperplasia (BPH)EpigeneticFibrosisSalmonella enterica (S. enterica)

Identifiers

PMID40442779
PMCPMC12121288

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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.