Evidence map›Paper›PMID 41194164›Full record

ArticleCell & bioscience2025

SETD7 exacerbates diabetic nephropathy through activating A

Qiuyuan Huang, Wen Zhong, Ruoxue Chen, Shenhan Xu, Huibin Wang, Jintao He, Yajie Hu, Honghong Chen, Chunxiang Fan, Xinhua Liu

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell & bioscience, 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. Article
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.

Qiuyuan Huang *Phenome Research Center of TCM, Department of Traditional Chinese Medicine, Shanghai Pudong Hospital; Pharmacophenomics Laboratory, Human Phenome Institute, Fudan University, Shanghai, 201203, China.
Wen Zhong *Phenome Research Center of TCM, Department of Traditional Chinese Medicine, Shanghai Pudong Hospital; Pharmacophenomics Laboratory, Human Phenome Institute, Fudan University, Shanghai, 201203, China.
Ruoxue ChenPhenome Research Center of TCM, Department of Traditional Chinese Medicine, Shanghai Pudong Hospital; Pharmacophenomics Laboratory, Human Phenome Institute, Fudan University, Shanghai, 201203, China.
Shenhan XuPhenome Research Center of TCM, Department of Traditional Chinese Medicine, Shanghai Pudong Hospital; Pharmacophenomics Laboratory, Human Phenome Institute, Fudan University, Shanghai, 201203, China.
Huibin WangPhenome Research Center of TCM, Department of Traditional Chinese Medicine, Shanghai Pudong Hospital; Pharmacophenomics Laboratory, Human Phenome Institute, Fudan University, Shanghai, 201203, China.
Jintao HePhenome Research Center of TCM, Department of Traditional Chinese Medicine, Shanghai Pudong Hospital; Pharmacophenomics Laboratory, Human Phenome Institute, Fudan University, Shanghai, 201203, China.
Yajie HuPhenome Research Center of TCM, Department of Traditional Chinese Medicine, Shanghai Pudong Hospital; Pharmacophenomics Laboratory, Human Phenome Institute, Fudan University, Shanghai, 201203, China.
Honghong ChenPhenome Research Center of TCM, Department of Traditional Chinese Medicine, Shanghai Pudong Hospital; Pharmacophenomics Laboratory, Human Phenome Institute, Fudan University, Shanghai, 201203, China.
Chunxiang FanPhenome Research Center of TCM, Department of Traditional Chinese Medicine, Shanghai Pudong Hospital; Pharmacophenomics Laboratory, Human Phenome Institute, Fudan University, Shanghai, 201203, China. fanxiang1258@163.com.
Xinhua LiuPhenome Research Center of TCM, Department of Traditional Chinese Medicine, Shanghai Pudong Hospital; Pharmacophenomics Laboratory, Human Phenome Institute, Fudan University, Shanghai, 201203, China. liuxinhua@fudan.edu.cn.ORCID http://orcid.org/0000-0002-9972-8215

Funding

Leading Talent Training Project of Shanghai Pudong New Area Health Commission PWRl2023-08Shanghai Pudong New Area Traditional Chinese Medicine Inheritance Innovation Development Demonstration Pilot Project YC-2023-0202 and YC-2023-0607
6 · The paper itself

Abstract

objectiveDiabetic nephropathy (DN) is a leading cause of end-stage renal disease (ESRD), and there has been growing attention towards the role of epigenetics in its pathogenesis. This study aims to investigate the underlying mechanism by which SET domain-containing lysine methyltransferase 7 (SETD7) modulates the progression of DN.

methodsSETD7 knockout mice (Setd7

resultsSETD7 expression was predominantly upregulated in high glucose-induced glomerular mesangial cells (MCs), and in diabetic mice kidney. Notably, SETD7 promoted the transcription of adenosine A

conclusionsOur results demonstrate an important role and mechanism of SETD7 in DN by promoting fibrosis and inflammation through the A2BR-mediated JAK2/STAT3 signaling pathway. Targeting SETD7 may represent a promising therapeutic strategy for halting the progression of DN.

Indexed as

A2BRDiabetic nephropathyJAK2/STAT3Mesangial cellsSETD7

Identifiers

PMID41194164
PMCPMC12590587

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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.