Evidence map›Paper›PMID 41169458›Full record

ArticleJournal of inflammation research2025

TIMP4 as a Potential Complementary Biomarker and Therapeutic Target in Membranous Nephropathy: A Multi-Omics Investigation with Clinical Validation.

Qingsong Chen, Gang Wang, Ruo Zhao, Qiyuan Hu, Jiayun Li, Yuting Wang, Jingyang Ran, Qi Huang, Guiquan Yu, Yanjia Luo and 1 more

Abstract read
In one paragraph

Article in Journal of inflammation research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
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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.

Qingsong ChenDepartment of Nephrology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, People's Republic of China.
Gang WangDepartment of Nephrology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, People's Republic of China.
Ruo ZhaoDepartment of Nephrology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, People's Republic of China.
Qiyuan HuDepartment of Nephrology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, People's Republic of China.
Jiayun LiDepartment of Nephrology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, People's Republic of China.
Yuting WangDepartment of Nephrology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, People's Republic of China.
Jingyang RanDepartment of Nephrology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, People's Republic of China.
Qi HuangDepartment of Nephrology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, People's Republic of China.
Guiquan YuDepartment of Nephrology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, People's Republic of China.
Yanjia LuoDepartment of Nephrology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, People's Republic of China.
Xiaohui LiaoDepartment of Nephrology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, People's Republic of China.ORCID 0000-0002-2329-0456

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Despite genome-wide association studies having revealed risk loci for membranous nephropathy (MN), the functional mechanisms linking genetic variants to disease pathogenesis remain poorly understood. Methods: We implemented a multi-stage analytical framework, integrating proteome-wide association studies (PWAS) and transcriptome-wide association studies (TWAS) to systematically prioritize MN-associated biomarkers. Genetic causality was rigorously established through summary data-based Mendelian randomization (SMR) and Bayesian colocalization analysis. Clinical validation was performed in a MN cohort. Additionally, single-cell transcriptomic profiling resolved cell-type-specific expression patterns of candidate targets. The therapeutic potential was further evaluated through drug target interaction and molecular docking. Results: PWAS identified three proteins associated with MN (PLA2R1, LY75, TIMP4), while TWAS of whole blood and kidney cortex tissues implicated significant associations for LY75, POLR2I, and NFKB1 in MN. TIMP4 was uniquely prioritized as a high-confidence candidate through concordant evidence from PWAS significance ( Conclusion: This study suggests TIMP4 may serve as a novel complementary biomarker and potential therapeutic target in MN. Systematic integration of multi-omics and clinical data provides promising insights for future drug development and mechanistic exploration.

Indexed as

genome-wide association studymembranous nephropathymulti-omicsproteome-wide association studytranscriptome-wide association study

Identifiers

PMID41169458
PMCPMC12570991

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