Evidence map›Paper›PMID 38258908›Full record

ArticleJCI insight2024

Integrin β1-rich extracellular vesicles of kidney recruit Fn1+ macrophages to aggravate ischemia-reperfusion-induced inflammation.

Wenjuan Wang, Xuejing Ren, Xiangmei Chen, Quan Hong, Guangyan Cai

Open access · goldAbstract 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 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
4.0field-weighted citation impact, top 6% of its field
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

18 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Macrophage-Fibroblast Crosstalk in Kidney Injury: A Narrative Review.International journal of molecular sciences · 2026
    Review
  3. Review
  4. Polysaccharide Peptide fromBiomolecules · 2026
    Article
  5. Cell-cell crosstalk in kidney health and disease.Nature reviews. Nephrology · 2026
    Review
  6. Article
  7. Article
  8. Review
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  10. Review
  11. Article
  12. Article
  13. Review
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  15. 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

5 authors at 3 institutions in 1 country.

Wenjuan WangSchool of Medicine, Nankai University, Tianjin, China.
Xuejing RenZhengzhou University People's Hospital, Henan Provincial People's Hospital, Henan Key Laboratory of Kidney Disease and Immunology, Zhengzhou, Henan, China.
Xiangmei ChenDepartment of Nephrology, First Medical Center of Chinese PLA General Hospital, National Key Laboratory of Kidney Diseases, National Clinical Research Center for Kidney Diseases, Beijing Key Laboratory of Kidney Diseases Research, Beijing, China.
Quan HongDepartment of Nephrology, First Medical Center of Chinese PLA General Hospital, National Key Laboratory of Kidney Diseases, National Clinical Research Center for Kidney Diseases, Beijing Key Laboratory of Kidney Diseases Research, Beijing, China.
Guangyan CaiSchool of Medicine, Nankai University, Tianjin, China.
Chinese PLA General Hospital · CNNankai University · CNHenan Provincial People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ischemia-reperfusion injury-induced (IRI-induced) acute kidney injury is accompanied by mononuclear phagocyte (MP) invasion and inflammation. However, systematic analysis of extracellular vesicle-carried (EV-carried) proteins mediating intercellular crosstalk in the IRI microenvironment is still lacking. Multiomics analysis combining single-cell RNA-Seq data of kidney and protein profiling of kidney-EV was used to elucidate the intercellular communication between proximal tubular cells (PTs) and MP. Targeted adhesion and migration of various MPs were caused by the secretion of multiple chemokines as well as integrin β1-rich EV by ischemic-damaged PTs after IRI. These recruited MPs, especially Fn1+ macrophagocyte, amplified the surviving PT's inflammatory response by secreting the inflammatory factors TNF-α, MCP-1, and thrombospondin 1 (THBS-1), which could interact with integrin β1 to promote more MP adhesion and interact with surviving PT to further promote the secretion of IL-1β. However, GW4869 reduced MP infiltration and maintained a moderate inflammatory level likely by blocking EV secretion. Our findings establish the molecular bases by which chemokines and kidney-EV mediate PT-MP crosstalk in early IRI and provide insights into systematic intercellular communication.

Indexed as

Integrin beta1KidneyAnimalsInflammationIschemiaReperfusionIntegrin beta1IntegrinsMacrophagesMonocytesNephrology

Identifiers

PMID38258908
PMCPMC10906229
OpenAlexW4391092435

What OpenQuestion holds

Textmetadata
LicenceCC BY
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 OpenQuestion graph.