Evidence map›Paper›PMID 40413560›Full record

ArticleBiomarker research2025

Single cell analysis identified IFN signaling activation contributes to the pathogenesis of pediatric steroid-sensitive nephrotic syndrome.

Qiu-Yu Li, Fei Liu, Xiaoyi Li, Minchao Kang, Linnan Bai, Tong Tong, Chen Zheng, Yanyan Jin, Xiaojing Zhang, Yi Xie and 7 more

Abstract read
In one paragraph

Article in Biomarker research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. 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

17 authors.

Qiu-Yu Li *Department of Nephrology, The Children's Hospital, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, No. 3333, Binsheng Road, Binjiang District, Hangzhou, Zhejiang, 310052, China.
Fei Liu *Department of Nephrology, The Children's Hospital, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, No. 3333, Binsheng Road, Binjiang District, Hangzhou, Zhejiang, 310052, China.
Xiaoyi Li *Department of Nephrology, The Children's Hospital, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, No. 3333, Binsheng Road, Binjiang District, Hangzhou, Zhejiang, 310052, China.
Minchao KangDepartment of Nephrology, Zhejiang University Medical College Affiliated Sir Run Run Shaw Hospital, Qingchun Road 3rd, Hangzhou, Zhejiang Province, 310016, China.
Linnan BaiDepartment of Nephrology, Zhejiang University Medical College Affiliated Sir Run Run Shaw Hospital, Qingchun Road 3rd, Hangzhou, Zhejiang Province, 310016, China.
Tong TongZhejiang University School of Medicine, Zhejiang University, 866 Yuhangtang Road, Hangzhou, Zhejiang, China.
Chen ZhengZhejiang University School of Medicine, Zhejiang University, 866 Yuhangtang Road, Hangzhou, Zhejiang, China.
Yanyan JinDepartment of Nephrology, The Children's Hospital, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, No. 3333, Binsheng Road, Binjiang District, Hangzhou, Zhejiang, 310052, China.
Xiaojing ZhangDepartment of Nephrology, The Children's Hospital, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, No. 3333, Binsheng Road, Binjiang District, Hangzhou, Zhejiang, 310052, China.
Yi XieDepartment of Nephrology, The Children's Hospital, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, No. 3333, Binsheng Road, Binjiang District, Hangzhou, Zhejiang, 310052, China.
Dandan TianDepartment of Clinical Laboratory, Children's Hospital, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, Hangzhou, China.
Yuanqing PanDepartment of Nephrology, Quanzhou Women's and Children's Hospital, Quanzhou, Fujian Province, 362000, China.
Jingjing WangDepartment of Nephrology, The Children's Hospital, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, No. 3333, Binsheng Road, Binjiang District, Hangzhou, Zhejiang, 310052, China.
Haidong FuDepartment of Nephrology, The Children's Hospital, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, No. 3333, Binsheng Road, Binjiang District, Hangzhou, Zhejiang, 310052, China.
Na JiaoState Key Laboratory of Genetic Engineering, Fudan Microbiome Center, School of Life Sciences, Fudan University, Shanghai, 200433, China.
Junnan WuDepartment of Nephrology, Zhejiang University Medical College Affiliated Sir Run Run Shaw Hospital, Qingchun Road 3rd, Hangzhou, Zhejiang Province, 310016, China. junnan.wu@zju.edu.cn.
JianHua MaoDepartment of Nephrology, The Children's Hospital, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, No. 3333, Binsheng Road, Binjiang District, Hangzhou, Zhejiang, 310052, China. maojh88@zju.edu.cn.

Funding

National Key Research and Development Program of China 2022YFC2505400National Key Research and Development Program of China 2022YFC2705103
6 · The paper itself

Abstract

backgroundIdiopathic nephrotic syndrome (INS) is a prevalent condition whose recurrence leads to multiple adverse effects. Previous studies on INS pathogenesis primarily focused on immune dysregulation, particularly T-cell changes and their correlation with cytokine shifts. Accumulating evidence suggests that B-cell dysfunction also plays a role. Nevertheless, a comprehensive understanding of the mechanisms and effective treatment strategies remains incomplete.

methodsThis study investigates changes in gene expressions and cellular interactions of immune cells at a single-cell level using peripheral blood mononuclear cells (PBMCs). And subsequently validated through quantitative PCR (qPCR), enzyme-linked immunosorbent assay (ELISA), and flow cytometry.

resultsWe identified seven main clusters using unsupervised clustering of 103,213 high-quality single cells. Through unsupervised clustering, patient-specific T cells (IFI44L + CD4 + T cells) that exhibited a pronounced elevation of interferon-stimulated genes (ISGs) is identified. Activation of ISGs and interferon (IFN)-related pathways are also observed in other clusters. Specifically, this study demonstrates that interferon-γ (IFN-γ) plays a crucial role by promoting the interaction between B-cell activating factor (BAFF) and receptors on B cells. This interaction triggers the release of autoantibodies, thereby initiating INS pathogenesis. Furthermore, telitacicept has shown efficacy in treating pediatric patients with frequent relapse NS(FRNS).

conclusionsOverall, our findings underscore the role of interferon and its related pathways in INS pathogenesis, providing novel therapeutic interventions for NS.

Indexed as

Idiopathic nephrotic syndromeIFNPBMCsscRNA-seq

Identifiers

PMID40413560
PMCPMC12103753

What Socratic holds

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LicenceCC BY
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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 Socratic graph.