Evidence map›Paper›PMID 38881891›Full record

ArticleFrontiers in immunology2024

Extracellular CIRP promotes Kupffer cell inflammatory polarization in sepsis.

Junji Shimizu, Atsushi Murao, Yongchan Lee, Monowar Aziz, Ping Wang

Abstract read
In one paragraph

Article in Frontiers in immunology, 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
–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

18 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. The Dual Role of Natural Killer Cells in the Septic Liver.Journal of inflammation research · 2026
    Review
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
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  16. Review
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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.

Junji ShimizuCenter for Immunology and Inflammation, The Feinstein Institutes for Medical Research, Manhasset, NY, United States.
Atsushi MuraoCenter for Immunology and Inflammation, The Feinstein Institutes for Medical Research, Manhasset, NY, United States.
Yongchan LeeCenter for Immunology and Inflammation, The Feinstein Institutes for Medical Research, Manhasset, NY, United States.
Monowar AzizCenter for Immunology and Inflammation, The Feinstein Institutes for Medical Research, Manhasset, NY, United States.
Ping WangCenter for Immunology and Inflammation, The Feinstein Institutes for Medical Research, Manhasset, NY, United States.

Funding

IMPROVEMENT OF ORGAN FUNCTION AFTER SEVERE HYPOVOLEMIAR01HL076179 · NHLBI · FEINSTEIN INSTITUTE FOR MEDICAL RESEARCH · PI PING WANG · 2004 to 2026
$7.6M
Novel Approaches to Maintaining Organ Function in SepsisR35GM118337 · NIGMS · FEINSTEIN INSTITUTE FOR MEDICAL RESEARCH · PI PING WANG · 2016 to 2026
$5.2M
Neutrophils in Sepsis: Role of CIRPR01GM129633 · NIGMS · FEINSTEIN INSTITUTE FOR MEDICAL RESEARCH · PI AZIZ, MONOWAR · 2018 to 2022
$1.6M
NHLBI NIH HHS R01 HL076179NIGMS NIH HHS R01 GM129633NIGMS NIH HHS R35 GM118337
6 · The paper itself

Abstract

Introduction: Sepsis is a life-threatening inflammatory condition caused by dysregulated host responses to infection. Extracellular cold-inducible RNA-binding protein (eCIRP) is a recently discovered damage-associated molecular pattern that causes inflammation and organ injury in sepsis. Kupffer cells can be activated and polarized to the inflammatory M1 phenotype, contributing to tissue damage by producing proinflammatory mediators. We hypothesized that eCIRP promotes Kupffer cell M1 polarization in sepsis. Methods: We stimulated Kupffer cells isolated from wild-type (WT) and TLR4 Results: eCIRP dose- and time-dependently increased IL-6 and TNFα release from WT Kupffer cells. In TLR4 Conclusion: Our data have clearly shown that eCIRP induces Kupffer cell M1 polarization via TLR4 pathway in sepsis, resulting in overproduction of inflammatory cytokines. eCIRP could be a promising therapeutic target to attenuate inflammation by preventing Kupffer cell M1 polarization in sepsis.

Indexed as

InflammationKupffer CellsRNA-Binding ProteinsSepsisAnimalsDisease Models, AnimalInterleukin-6MaleMannose ReceptorMiceMice, Inbred C57BLMice, KnockoutNitric Oxide Synthase Type IIToll-Like Receptor 4Tumor Necrosis Factor-alphaCirbp protein, mouseInterleukin-6Mannose ReceptorNitric Oxide Synthase Type IIRNA-Binding ProteinsTlr4 protein, mouseToll-Like Receptor 4Tumor Necrosis Factor-alphaacute liver injuryeCIRPKupffer cellM1sepsis

Identifiers

PMID38881891
PMCPMC11177612

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.