Evidence map›Paper›PMID 41376641›Full record

ArticleFrontiers in immunology2025

IgA expressed by glomerular mesangial cells is involved in the pathogenesis of IgA nephropathy.

Haidong Zhang, Zhenling Deng, Yueming Gao, Qi Li, Lu Zhang, Yue Wang

Abstract read
In one paragraph

Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

6 authors.

Haidong Zhang *Department of Nephrology, Peking University Third Hospital, Beijing, China.
Zhenling Deng *Department of Nephrology, Peking University Third Hospital, Beijing, China.
Yueming GaoDepartment of Nephrology, Peking University Third Hospital, Beijing, China.
Qi LiDepartment of Nephrology, Peking University Third Hospital, Beijing, China.
Lu ZhangDepartment of Nephrology, Peking University Third Hospital, Beijing, China.
Yue WangDepartment of Nephrology, Peking University Third Hospital, Beijing, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: The widely accepted "multi-hit hypothesis" of IgAN pathogenesis was challenged, as efficient depletion of CD20+ B cells failed to reduce serum galactose-deficient IgA1 (Gd-IgA1) or proteinuria in IgAN patients. Our group has discovered glomerular mesangial cells (GMCs) as another source of IgA, while immunoglobulin produced by non-B cells (non-B Ig) participating in several inflammatory and neoplastic diseases arose as a new concept in immunology. It is still unclear whether IgA produced by GMCs participates in the pathogenesis of IgAN and what its preliminary mechanism is. Methods: The transcription of Results: Expression of IgA in GMCs was reconfirmed by detecting Conclusion: We reconfirmed the expression of IgA in GMCs and demonstrated that overexpression of Gd-IgA1 in GMCs induced by SEB through the TLR4 pathway in human GMC may play an important role in inducing an inflammatory response in IgAN.

Indexed as

Glomerulonephritis, IGAImmunoglobulin AMesangial CellsAnimalsB-LymphocytesDisease Models, AnimalHumansMaleMiceMice, Inbred C57BLMice, KnockoutToll-Like Receptor 4Immunoglobulin AToll-Like Receptor 4galactose-deficient IgA1GMC conditional IGHA knockout miceIgA nephropathynon-B immunoglobulinμMT mice

Identifiers

PMID41376641
PMCPMC12685827

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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.