Evidence map›Paper›PMID 32790017›Full record

ArticleJournal of cellular and molecular medicine2020

Role of CARD9 in inflammatory signal pathway of peritoneal macrophages in severe acute pancreatitis.

Jing Wang, Jun Tian, Yang-Huan He, Zhi-Wen Yang, Lin Wang, Yue-Xing Lai, Ping Xu

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

8 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. CARD9 Mediates Pancreatic Islet Beta-Cell Dysfunction Under the Duress of Hyperglycemic Stress.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2022
    Article
  6. CARD9 Signaling, Inflammation, and Diseases.Frontiers in immunology · 2022
    Review
  7. Article
  8. 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

7 authors at 3 institutions in 1 country.

Jing WangSongjiang Hospital Affiliated to Shanghai Jiaotong University School of Medicine (Preparatory Stage), Shanghai, China.
Jun TianSongjiang Hospital Affiliated to Shanghai Jiaotong University School of Medicine (Preparatory Stage), Shanghai, China.
Yang-Huan HeJinshan Hospital of Fudan University, Shanghai, China.
Zhi-Wen YangSongjiang Hospital Affiliated to Shanghai Jiaotong University School of Medicine (Preparatory Stage), Shanghai, China.ORCID 0000-0001-7354-9617
Lin WangShanghai Songjiang Clinical Medical College of Nanjing Medical University, Nanjing, China.
Yue-Xing LaiSongjiang Hospital Affiliated to Shanghai Jiaotong University School of Medicine (Preparatory Stage), Shanghai, China.
Ping XuSongjiang Hospital Affiliated to Shanghai Jiaotong University School of Medicine (Preparatory Stage), Shanghai, China.ORCID 0000-0003-0270-9841
Songjiang District Central Hospital · CNJinshan Hospital of Fudan University · CNNanjing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Previous studies revealed that caspase recruitment domain protein 9 (CARD9) was involved in severe acute pancreatitis (SAP) inflammation and that interfering with its expression in vivo could inhibit inflammation. However, the specific mechanism is unknown. This study aimed to discover the related signal pathways of CARD9 in macrophages. SiRNA interference technology was used in vivo and in vitro to detect CARD9-related signal pathways in peritoneal macrophages. Furthermore, Toll-like receptor 4 (TLR4) and membrane-associated C-type lectin-1 (Dectin-1) pathways in macrophages were activated specially to looking for the upstream signal path of CARD9. Results showed up-regulation of CARD9 expression in peritoneal macrophages of SAP rats (P < .05). CARD9 siRNA alleviated inflammatory cytokines, and inhibited the phosphorylation of NF-κB and p38MAPK in peritoneal macrophages in vivo or in vitro. Meanwhile, CARD9 siRNA reduced the concentration of CARD9 and Bcl10 in peritoneal macrophages, and TLR4 and Dectin-1 took part in CARD9 signal pathways in macrophages. In conclusion, there is an inflammation signal pathway comprised of TLR4/Dectin-1-CARD9-NF-κB/p38MAPK activated in macrophages in SAP. Blockade of CARD9 expression in macrophages can effectively alleviate SAP inflammation.

Indexed as

AnimalsCARD Signaling Adaptor ProteinsDectin-1Disease Models, AnimalGene Expression RegulationHumansInflammationLectins, C-TypeMacrophagesNF-kappa Bp38 Mitogen-Activated Protein KinasesPancreatitisPeritoneumRatsRNA, Small InterferingSeverity of Illness IndexCard9 protein, ratCARD Signaling Adaptor ProteinsDectin-1Lectins, C-TypeNF-kappa Bp38 Mitogen-Activated Protein KinasesRNA, Small InterferingTlr4 protein, ratToll-Like Receptor 4caspase recruitment domain-containing protein 9Dectin-1macrophagessevere acute pancreatitistoll-like receptor 4

Identifiers

PMID32790017
PMCPMC7520331
OpenAlexW3048706602

What OpenQuestion holds

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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.