Evidence map›Paper›PMID 38716725›Full record

ArticleJCI insight2024

Cross-species single-cell analysis uncovers the immunopathological mechanisms associated with IgA nephropathy progression.

Xizhao Chen, Tiantian Wang, Lei Chen, Yinghua Zhao, Yiyao Deng, Wanjun Shen, Lin Li, Zhong Yin, Chaoran Zhang, Guangyan Cai and 2 more

Abstract read
In one paragraph

Article in JCI insight, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing 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

20 citing papers in PubMed.

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  12. TREM2Experimental physiology · 2025
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  16. Research (Washington, D.C.) · 2025
    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

12 authors.

Xizhao ChenDepartment of Nephrology, The First Medical Center of Chinese People's Liberation Army General Hospital, Nephrology Institute of the Chinese People's Liberation Army, State Key Laboratory of Kidney Diseases, National Clinical Research Center for Kidney Diseases, Beijing Key Laboratory of Kidney Disease Research, Beijing, China.
Tiantian WangDepartment of Nephrology, The First Medical Center of Chinese People's Liberation Army General Hospital, Nephrology Institute of the Chinese People's Liberation Army, State Key Laboratory of Kidney Diseases, National Clinical Research Center for Kidney Diseases, Beijing Key Laboratory of Kidney Disease Research, Beijing, China.
Lei ChenDepartment of Critical Care Nephrology and Blood Purification, the First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
Yinghua ZhaoBeijing Tsinghua Changgung Hospital, School of Clinical Medicine, Tsinghua University, Beijing, China.
Yiyao DengDepartment of Nephrology, Guizhou Provincial People's Hospital, Guiyang, China.
Wanjun ShenDepartment of Nephrology, The First Medical Center of Chinese People's Liberation Army General Hospital, Nephrology Institute of the Chinese People's Liberation Army, State Key Laboratory of Kidney Diseases, National Clinical Research Center for Kidney Diseases, Beijing Key Laboratory of Kidney Disease Research, Beijing, China.
Lin LiDepartment of Nephrology, The First Medical Center of Chinese People's Liberation Army General Hospital, Nephrology Institute of the Chinese People's Liberation Army, State Key Laboratory of Kidney Diseases, National Clinical Research Center for Kidney Diseases, Beijing Key Laboratory of Kidney Disease Research, Beijing, China.
Zhong YinDepartment of Nephrology, The First Medical Center of Chinese People's Liberation Army General Hospital, Nephrology Institute of the Chinese People's Liberation Army, State Key Laboratory of Kidney Diseases, National Clinical Research Center for Kidney Diseases, Beijing Key Laboratory of Kidney Disease Research, Beijing, China.
Chaoran ZhangDepartment of Stomatology, The First Medical Center of People's Liberation Army General Hospital, Beijing, China.
Guangyan CaiDepartment of Nephrology, The First Medical Center of Chinese People's Liberation Army General Hospital, Nephrology Institute of the Chinese People's Liberation Army, State Key Laboratory of Kidney Diseases, National Clinical Research Center for Kidney Diseases, Beijing Key Laboratory of Kidney Disease Research, Beijing, China.
Min ZhangDepartment of Nephrology, The First Medical Center of Chinese People's Liberation Army General Hospital, Nephrology Institute of the Chinese People's Liberation Army, State Key Laboratory of Kidney Diseases, National Clinical Research Center for Kidney Diseases, Beijing Key Laboratory of Kidney Disease Research, Beijing, China.
Xiangmei ChenDepartment of Nephrology, The First Medical Center of Chinese People's Liberation Army General Hospital, Nephrology Institute of the Chinese People's Liberation Army, State Key Laboratory of Kidney Diseases, National Clinical Research Center for Kidney Diseases, Beijing Key Laboratory of Kidney Disease Research, Beijing, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

IgA nephropathy (IgAN) represents the main cause of renal failure, while the precise pathogenetic mechanisms have not been fully determined. Herein, we conducted a cross-species single-cell survey on human IgAN and mouse and rat IgAN models to explore the pathogenic programs. Cross-species single-cell RNA sequencing (scRNA-Seq) revealed that the IgAN mesangial cells (MCs) expressed high levels of inflammatory signatures CXCL12, CCL2, CSF1, and IL-34 and specifically interacted with IgAN macrophages via the CXCL12/CXCR4, CSF1/IL-34/CSF1 receptor, and integrin subunit alpha X/integrin subunit alpha M/complement C3 (C3) axes. IgAN macrophages expressed high levels of CXCR4, PDGFB, triggering receptor expressed on myeloid cells 2, TNF, and C3, and the trajectory analysis suggested that these cells derived from the differentiation of infiltrating blood monocytes. Additionally, protein profiling of 21 progression and 28 nonprogression IgAN samples revealed that proteins CXCL12, C3, mannose receptor C-type 1, and CD163 were negatively correlated with estimated glomerular filtration rate (eGFR) value and poor prognosis (30% eGFR as composite end point). Last, a functional experiment revealed that specific blockade of the Cxcl12/Cxcr4 pathway substantially attenuated the glomerulus and tubule inflammatory injury, fibrosis, and renal function decline in the mouse IgAN model. This study provides insights into IgAN progression and may aid in the refinement of IgAN diagnosis and the optimization of treatment strategies.

Indexed as

Disease ProgressionGlomerulonephritis, IGAMacrophagesSingle-Cell AnalysisAdultAnimalsChemokine CXCL12Disease Models, AnimalFemaleGlomerular Filtration RateHumansInterleukinsMaleMesangial CellsMiceRatsChemokine CXCL12CXCL12 protein, humanCXCR4 protein, humanIL34 protein, humanInterleukinsReceptors, CXCR4Autoimmune diseasesAutoimmunityBioinformaticsChemokinesImmunology

Identifiers

PMID38716725
PMCPMC11141938

What OpenQuestion holds

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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 OpenQuestion graph.