Evidence map›Paper›PMID 37905652›Full record

ArticleIn vivo (Athens, Greece)

Thiamet G as a Potential Treatment for Polycystic Kidney Disease.

Wen-Cheng Su, Chi-Feng Hung, Yi-Chieh Wang, Hubert Peng, Wen-Hung Huang, Yi-Lun Lo, Yun-Hwa Lo, Yi-Cheng Chen, Hsin-Hui Su, Yung-Liang Chen

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in In vivo (Athens, Greece). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.9field-weighted citation impact, top 19% 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

4 citing papers in PubMed, 3 citations in OpenAlex.

  1. Review
  2. TargetingbioRxiv : the preprint server for biology · 2025
    Article
  3. Article
  4. Immunohistochemical Study onActa histochemica et cytochemica · 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

10 authors at 7 institutions in 1 country.

Wen-Cheng Su *Department of Medical Laboratory Science and Biotechnology, Yuan Pei University of Medical Technology, Hsinchu, Taiwan, R.O.C.
Chi-Feng Hung *Department of Urology, Ditmanson Medical Foundation Chia-yi Christian Hospital, Chia-Yi City, Taiwan, R.O.C.
Yi-Chieh WangDepartment of Biochemistry and Molecular Biology, College of Medicine, National Cheng Kung University, Tainan, Taiwan, R.O.C.
Hubert PengInstitute of Molecular Biology, Academia Sinica, Taipei, Taiwan, R.O.C.
Wen-Hung HuangInstitute of Pharmacology, College of Medicine, National Yang Ming Chiao Tung University, Taipei, Taiwan, R.O.C.
Yi-Lun LoDepartment of Medicinal and Applied Chemistry, College of Life Science, Kaohsiung Medical University, Kaohsiung, Taiwan, R.O.C.
Yun-Hwa LoDepartment of Veterinary Medicine, National Pingtung University of Science and Technology, Pingtung, Taiwan, R.O.C.
Yi-Cheng ChenDepartment of Biochemistry and Molecular Biology, College of Medicine, National Cheng Kung University, Tainan, Taiwan, R.O.C.
Hsin-Hui Su *Department of Pharmacy, Chia Nan University of Pharmacy and Science, Tainan, Taiwan, R.O.C. hsinhuisu@gm.cnu.edu.tw.
Yung-Liang Chen *Department of Medical Laboratory Science and Biotechnology, Yuan Pei University of Medical Technology, Hsinchu, Taiwan, R.O.C.; yuangliang@mail.ypu.edu.tw.
Yuanpei University · TWKaohsiung Medical University · TWChia Nan University of Pharmacy and Science · TWChia-Yi Christian Hospital · TWInstitute of Molecular Biology, Academia Sinica · TWNational Cheng Kung University · TWNational Yang Ming Chiao Tung University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND/

aimAutosomal dominant polycystic kidney disease (ADPKD) is a prevalent genetic disorder primarily caused by mutations in Pkd1 (PC1), which account for the majority of ADPKD cases. These mutations contribute to the formation of cysts in the kidneys and other organs, ultimately leading to renal failure. Unfortunately, there are currently no available preventive treatments for this disease. MATERIALS AND

methodsIn this study, we utilized Pkd1-knockdown mice and cells to investigate the potential involvement of O-GlcNAcylation in the progression of PKD. Additionally, we examined the effects of thiamet G, an inhibitor of O-GlcNAcase (OGA), on PKD mice.

resultsOur findings indicate that both O-GlcNAcylation and OGT (O-GlcNAc transferase) were downregulated in the renal tissues of Pkd1-silenced mice. Furthermore, O-GlcNAcylation was shown to regulate the stability and function of the C-terminal cytoplasmic tail (CTT) of PC1. Treatment of PKD mice with thiamet G resulted in a reduction of renal cytogenesis in these animals.

conclusionThese results highlight the unique role of O-GlcNAcylation in the development of cyst formation in PKD and propose it as a potential therapeutic target for the treatment of PKD.

Indexed as

Polycystic Kidney, Autosomal DominantPolycystic Kidney DiseasesAnimalsKidneyMicePyransThiazolesPyransthiamet GThiazolesADPKDAutosomal dominant polycystic kidney diseaseO-linked N-acetylglucosamineThiamet G

Identifiers

PMID37905652
PMCPMC10621443
OpenAlexW4388033238

What Socratic holds

Textmetadata
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 Socratic graph.