Evidence map›Paper›PMID 38195664›Full record

ArticleCell death discovery2024

The E3 ubiquitin ligase TRIM39 modulates renal fibrosis induced by unilateral ureteral obstruction through regulating proteasomal degradation of PRDX3.

Jun Jian, Yunxun Liu, Qingyuan Zheng, Jingsong Wang, Zhengyu Jiang, Xiuheng Liu, Zhiyuan Chen, Shanshan Wan, Hao Liu, Lei Wang

Open access · goldAbstract read
In one paragraph

Article in Cell death discovery, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

10 citing papers in PubMed, 12 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. The TRIM14-KIF1B Axis Drives Renal Injury in Diabetic Nephropathy Through TLR4/NF-κB Pathway Modulation.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026
    Article
  5. Article
  6. Article
  7. Machine Learning-Driven Discovery of TRIM Genes as Diagnostic Biomarkers for Idiopathic Pulmonary Fibrosis.Medical science monitor : international medical journal of experimental and clinical research · 2025
    Article
  8. Article
  9. Review
  10. 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 1 institution in 1 country.

Jun Jian *Department of Urology, Renmin Hospital of Wuhan University, Wuhan, 430060, Hubei, China.
Yunxun Liu *Department of Urology, Renmin Hospital of Wuhan University, Wuhan, 430060, Hubei, China.
Qingyuan Zheng *Department of Urology, Renmin Hospital of Wuhan University, Wuhan, 430060, Hubei, China.ORCID http://orcid.org/0000-0003-4682-3857
Jingsong WangDepartment of Urology, Renmin Hospital of Wuhan University, Wuhan, 430060, Hubei, China.
Zhengyu JiangDepartment of Urology, Renmin Hospital of Wuhan University, Wuhan, 430060, Hubei, China.
Xiuheng LiuDepartment of Urology, Renmin Hospital of Wuhan University, Wuhan, 430060, Hubei, China.
Zhiyuan ChenDepartment of Urology, Renmin Hospital of Wuhan University, Wuhan, 430060, Hubei, China.
Shanshan WanDepartment of Ophthalmology, Renmin Hospital of Wuhan University, Wuhan, 430060, Hubei, China. ophwss@whu.edu.cn.
Hao LiuDepartment of Urology, Renmin Hospital of Wuhan University, Wuhan, 430060, Hubei, China. liuhao269@163.com.
Lei WangDepartment of Urology, Renmin Hospital of Wuhan University, Wuhan, 430060, Hubei, China. drwanglei@whu.edu.cn.ORCID http://orcid.org/0000-0001-8412-1130
Wuhan University · CN

Funding

École Nationale d'Ingénieurs de Saint-Etienne (National Engineering School of Saint-Étienne) 82000639National Natural Science Foundation of China (National Science Foundation of China) 82300782
6 · The paper itself

Abstract

Renal fibrosis is considered to be the ultimate pathway for various chronic kidney disease, with a complex etiology and great therapeutic challenges. Tripartite motif-containing (TRIM) family proteins have been shown to be involved in fibrotic diseases, but whether TRIM39 plays a role in renal fibrosis remain unexplored. In this study, we investigated the role of TRIM39 in renal fibrosis and its molecular mechanism. TRIM39 expression was analyzed in patients' specimens, HK-2 cells and unilateral ureteral obstruction (UUO) mice were used for functional and mechanistic studies. We found an upregulated expression of TRIM39 in renal fibrosis human specimens and models. In addition, TRIM39 knockdown was found efficient for alleviating renal fibrosis in both UUO mice and HK-2 cells. Mechanistically, we demonstrated that TRIM39 interacted with PRDX3 directly and induced ubiquitination degradation of PRDX3 at K73 and K149 through the K48 chain, which resulted in ROS accumulation and increased inflammatory cytokine generation, and further aggravated renal fibrosis. It provided an emerging potential target for the therapies of renal fibrosis.

Identifiers

PMID38195664
PMCPMC10776755
OpenAlexW4390727588

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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.