Evidence map›Paper›PMID 20823759›Full record

ArticleAnesthesiology2010

Caspase-1 modulates incisional sensitization and inflammation.

De-Yong Liang, XiangQi Li, Wen-Wu Li, Dennis Fiorino, Yanli Qiao, Peyman Sahbaie, David C Yeomans, J David Clark

Open access · bronzeAbstract read
In one paragraph

Article in Anesthesiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
3.8field-weighted citation impact, top 8% 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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Alcohol accumulation promotes esophagitis via pyroptosis activation.International journal of biological sciences · 2018
    Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

8 authors at 3 institutions in 1 country.

De-Yong LiangDepartment of Anesthesiology, Veterans Affairs Palo Alto Health Care System, Palo Alto, California, USA.
XiangQi Li
Wen-Wu Li
Dennis Fiorino
Yanli Qiao
Peyman Sahbaie
David C Yeomans
J David Clark
Stanford University · USVA Palo Alto Health Care System · USVertex Pharmaceuticals (United States) · US

Funding

Complement System Modulation of Nociception and Inflammation after IncisionR01GM079126 · NIGMS · PALO ALTO VETERANS INSTIT FOR RESEARCH · PI CLARK, DAVID J. · 2008 to 2011
$1.4M
NIGMS NIH HHS GM079126NIGMS NIH HHS R01 GM079126
6 · The paper itself

Abstract

backgroundSurgical injury induces production and release of inflammatory mediators in the vicinity of the wound. They in turn trigger nociceptive signaling to produce hyperalgesia and pain. Interleukin-1β plays a crucial role in this process. The mechanism regulating production of this cytokine after incision is, however, unknown. Caspase-1 is a key enzyme that cleaves prointerleukin-1β to its active form. We hypothesized that caspase-1 is a crucial regulator of incisional interleukin-1β levels, nociceptive sensitization, and inflammation.

methodsThese studies employed a mouse hind paw incisional model. Caspase-1 was blocked using the selective inhibitors Ac-YVAD-CMK and VRTXSD727. Nociceptive sensitization, edema, and hind paw warmth were followed in intact animals whereas caspase-1 activity, cytokine, and prostaglandin E2 levels were assessed in homogenized skin. Confocal microscopy was used to detect the expression of caspase-1 near the wounds.

resultsAnalysis of enzyme activity demonstrated that caspase-1 activity was significantly increased in periincisional skin. Pretreatment with Ac-YVAD-CMK significantly reduced mechanical allodynia and thermal hyperalgesia. Repeated administration of this inhibitor produced robust analgesia, especially to mechanical stimulation. Administration of VRTXSD727 provided qualitatively similar results. Caspase-1 inhibition also reduced edema and the normally observed increase in paw warmth around the wound site. Correspondingly, caspase-1 inhibition significantly reduced interleukin-1β as well as macrophage-inflammatory protein 1α, granulocyte colony-stimulating factor, and prostaglandin E2 levels near the wound. The expression of caspase-1 was primarily observed in keratinocytes in the epidermal layer and in neutrophils deeper in the wounds.

conclusionsThe current study demonstrates that the inhibition of caspase-1 reduces postsurgical sensitization and inflammation, likely through a caspase-1/interleukin-1β-dependent mechanism.

Indexed as

AnimalsBiomarkersBody TemperatureCaspase 1Caspase InhibitorsChemokine CCL3DinoprostoneEdemaGranulocyte Colony-Stimulating FactorHindlimbHot TemperatureHyperalgesiaImmunohistochemistryInflammationInterleukin-1betaMaleBiomarkersCaspase 1Caspase InhibitorsCcl3 protein, mouseChemokine CCL3DinoprostoneGranulocyte Colony-Stimulating FactorInterleukin-1beta

Identifiers

PMID20823759
PMCPMC2945456
OpenAlexW2042600705

What OpenQuestion holds

Textmetadata
LicenceTDM
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.