Evidence map›Paper›PMID 39472935›Full record

ArticleJournal of translational medicine2024

EZH2 inhibition or genetic ablation suppresses cyst growth in autosomal dominant polycystic kidney disease.

Jiayi Lv, Bingxue Lan, Lili Fu, Chaoran He, Wei Zhou, Xi Wang, Chenchen Zhou, Zhiguo Mao, Yupeng Chen, Changlin Mei and 1 more

Abstract read
In one paragraph

Article in Journal of translational medicine, 2024. 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
–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

8 citing papers in PubMed.

  1. Review
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  5. Article
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  7. Article
  8. Protein lactylation in kidney diseases.Frontiers in cell and developmental biology · 2025
    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.

Jiayi Lv *Kidney Institute, Division of Nephrology, Shanghai Changzheng Hospital, Second Military Medical University (Naval Medical University), 415 Fengyang Road, Shanghai, 200003, China.
Bingxue Lan *Center for Clinical Laboratories, Affiliated Hospital of Guizhou Medical University, Guiyang City, Guizhou Province, China.
Lili Fu *Kidney Institute, Division of Nephrology, Shanghai Changzheng Hospital, Second Military Medical University (Naval Medical University), 415 Fengyang Road, Shanghai, 200003, China.
Chaoran HeDepartment of Biochemistry and Molecular Biology, 2011 Collaborative Innovation Center of Tianjin for Medical Epigenetics, Tianjin Key Laboratory of Medical Epigenetics, School of Basic Medical Sciences, Tianjin Medical University, 22 Qixiangtai Road, Tianjin, 300070, China.
Wei ZhouDepartment of Nephrology, Shanghai General Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, 200080, China.
Xi WangInstitute of Infectious Diseases, Beijing Key Laboratory of Emerging Infectious Diseases, Beijing Ditan Hospital, Capital Medical University, Beijing, 100015, China.
Chenchen ZhouOutpatient Department, Yangpu Third Military Retreat, Shanghai, China.
Zhiguo MaoKidney Institute, Division of Nephrology, Shanghai Changzheng Hospital, Second Military Medical University (Naval Medical University), 415 Fengyang Road, Shanghai, 200003, China. maozhiguo93@163.com.
Yupeng ChenDepartment of Biochemistry and Molecular Biology, 2011 Collaborative Innovation Center of Tianjin for Medical Epigenetics, Tianjin Key Laboratory of Medical Epigenetics, School of Basic Medical Sciences, Tianjin Medical University, 22 Qixiangtai Road, Tianjin, 300070, China. ychen@tmu.edu.cn.
Changlin MeiKidney Institute, Division of Nephrology, Shanghai Changzheng Hospital, Second Military Medical University (Naval Medical University), 415 Fengyang Road, Shanghai, 200003, China. changlinmei@smmu.edu.cn.
Cheng XueKidney Institute, Division of Nephrology, Shanghai Changzheng Hospital, Second Military Medical University (Naval Medical University), 415 Fengyang Road, Shanghai, 200003, China. chengxia1568@126.com.ORCID 0000-0002-4132-9406

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAutosomal Dominant Polycystic Kidney Disease (ADPKD) is a prevalent genetic disorder characterized by the formation of renal cysts leading to kidney failure. Despite known genetic underpinnings, the variability in disease progression suggests additional regulatory layers, including epigenetic modifications.

methodsWe utilized various ADPKD models, including Pkd1 and Ezh2 conditional knockout (Pkd1

resultsEZH2 expression was significantly upregulated in Pkd1

conclusionOur findings elucidate the pivotal role of EZH2 in promoting renal cyst growth through epigenetic mechanisms and suggest that EZH2 inhibition or ablation may serve as a novel therapeutic approach for managing ADPKD.

Indexed as

Enhancer of Zeste Homolog 2 ProteinPolycystic Kidney, Autosomal DominantAnimalsCystsDisease Models, AnimalDogsHumansIndolesKidneyMadin Darby Canine Kidney CellsMiceMice, KnockoutPyridonesSignal TransductionTRPP Cation ChannelsEnhancer of Zeste Homolog 2 ProteinEzh2 protein, mouseGSK-2816126IndolesPyridonesTRPP Cation ChannelsAutosomal dominantEnhancer of zeste homolog 2EpigeneticsFerroptosisp21Polycystic kidney disease

Identifiers

PMID39472935
PMCPMC11520870

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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.