Evidence mapPaperPMID 40506482Full record

ArticleCommunications biology2025

Inflammation-associated molecules in the glomerular-endothelium in mild IgA-nephropathy patients identified by single-cell and spatial transcriptome.

Kumi Hasegawa, Nagako Kawashima, Ayako Kawabata, Megumi Sakakura, Naoki Onoda, Takashi Sano, Itaru Urakawa, Masahiro Matsubara, Shokichi Naito

Abstract read
In one paragraph

Article in Communications biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
  4. 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

9 authors.

Kumi HasegawaResearch Core Function Laboratories, Research Division, Kyowa Kirin Co., Ltd., 3-6-6, Asahi-machi, Machida-shi, Tokyo, 194-8533, Japan. kumi.hasegawa.wj@kyowakirin.com.ORCID http://orcid.org/0000-0002-6299-8369
Nagako KawashimaDepartment of Nephrology, School of Medicine, Kitasato University, 1-15-1 Kitasato, Minami-ku, Sagamihara-shi, Kanagawa, 252-0374, Japan.
Ayako KawabataResearch Core Function Laboratories, Research Division, Kyowa Kirin Co., Ltd., 3-6-6, Asahi-machi, Machida-shi, Tokyo, 194-8533, Japan.
Megumi SakakuraModality Research Laboratories 1, Research Division, Kyowa Kirin Co., Ltd., 3-6-6, Asahi-machi, Machida-shi, Tokyo, 194-8533, Japan.
Naoki OnodaResearch Core Function Laboratories, Research Division, Kyowa Kirin Co., Ltd., 3-6-6, Asahi-machi, Machida-shi, Tokyo, 194-8533, Japan.ORCID http://orcid.org/0000-0001-6612-1129
Takashi SanoDepartment of Nephrology, School of Medicine, Kitasato University, 1-15-1 Kitasato, Minami-ku, Sagamihara-shi, Kanagawa, 252-0374, Japan.
Itaru UrakawaTokyo Research Park, Research Division, Kyowa Kirin Co., Ltd., 3-6-6, Asahi-machi, Machida-shi, Tokyo, 194-8533, Japan.
Masahiro MatsubaraResearch Core Function Laboratories, Research Division, Kyowa Kirin Co., Ltd., 3-6-6, Asahi-machi, Machida-shi, Tokyo, 194-8533, Japan.
Shokichi NaitoDepartment of Nephrology, School of Medicine, Kitasato University, 1-15-1 Kitasato, Minami-ku, Sagamihara-shi, Kanagawa, 252-0374, Japan. snaito@med.kitasato-u.ac.jp.ORCID http://orcid.org/0009-0007-5715-7534

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Immunoglobulin A nephropathy (IgA-N) is a primary glomerulonephritis that is characterized by mesangial cell proliferation and expansion. Although glomerular endothelial cells (GE) are implicated in the pathogenesis of IgA-N, their role remains poorly understood. We conduct single-cell and spatial transcriptomic analysis using human specimens with mild IgA-N compared with normal. We integrate single-cell and spatial transcriptome analyses in human samples of mild IgA-N compared to normal samples, revealing several novel findings: (1) identification of clusters of GE and their expressed gene profiles, (2) identification of novel inflammation-related molecules newly implicated in GE in mild IgA-N, (3) activation of inflammatory pathways characteristic of IgA-N. Therefore, we suggest the importance of GE in the mechanism of IgA-N, as GE initiates more active inflammatory response prior to mesangial cells in patients with mild IgA-N. These findings provide useful information for understanding the pathogenesis and choosing the best drug for IgA nephropathy.

Indexed as

Endothelial CellsGlomerulonephritis, IGAInflammationKidney GlomerulusTranscriptomeAdultFemaleGene Expression ProfilingHumansMaleMiddle AgedSingle-Cell Analysis

Identifiers

PMID40506482
PMCPMC12162889

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.