Evidence map›Paper›PMID 24449582›Full record

ArticleArthritis & rheumatology (Hoboken, N.J.)2014

An essential role of caspase 1 in the induction of murine lupus and its associated vascular damage.

J Michelle Kahlenberg, Srilakshmi Yalavarthi, Wenpu Zhao, Jeffrey B Hodgin, Tamra J Reed, Noriko M Tsuji, Mariana J Kaplan

Open access · bronzeAbstract read
In one paragraph

Article in Arthritis & rheumatology (Hoboken, N.J.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

55 citing papers in PubMed, 92 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Vascular damage in systemic lupus erythematosus.Nature reviews. Nephrology · 2024
    Review
  8. The P2X7 Receptor in Autoimmunity.International journal of molecular sciences · 2023
    Review
  9. Article
  10. Article
  11. The Role of Inflammasomes in Glomerulonephritis.International journal of molecular sciences · 2022
    Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 2 countries.

J Michelle KahlenbergUniversity of Michigan, Ann Arbor.
Srilakshmi Yalavarthi
Wenpu Zhao
Jeffrey B Hodgin
Tamra J Reed
Noriko M Tsuji
Mariana J Kaplan
University of Michigan–Ann Arbor · USNational Institute of Advanced Industrial Science and Technology · JP

Funding

Systemic AutoimmunityZIAAR041199 · NIAMS · NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES · PI KAPLAN, MARIANA · 2014 to 2025
$32.5M
NETs in the development of lupus and its cardiovascular complicationsR01HL088419 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI EITZMAN, DANIEL T · 2009 to 2016
$3.1M
The Rho GTPases Cdc42 and Rac1 in diabetic NephropathyK08DK088944 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI HODGIN, JEFFREY BENTON · 2010 to 2014
$767k
NHLBI NIH HHS HL-088419NHLBI NIH HHS R01 HL088419NIDDK NIH HHS K08 DK088944NIDDK NIH HHS K08-DK-088944
6 · The paper itself

Abstract

objectiveSystemic lupus erythematosus (SLE) is a systemic autoimmune syndrome associated with organ damage and an elevated risk of cardiovascular disease resulting from activation of both innate and adaptive immune pathways. Recently, increased activation of the inflammasome machinery in SLE has been described. Using the mouse model of pristane-induced lupus, we undertook this study to explore whether caspase 1, the central enzyme of the inflammasome, plays a role in the development of SLE and its associated vascular dysfunction.

methodsEight-week-old wild-type (WT) or caspase 1(-/-) mice were injected intraperitoneally with phosphate buffered saline or pristane. Six months after injection, mice were euthanized, and the development of a lupus phenotype and vascular dysfunction was assessed.

resultsWhile WT mice exposed to pristane developed autoantibodies and a strong type I interferon response, mice lacking caspase 1 were significantly protected against these features as well as against pristane-induced vascular dysfunction. Further, the development of immune complex glomerulonephritis, which was prominent after pristane exposure in WT mice, was significantly abrogated in caspase 1(-/-) mice.

conclusionThese results indicate that caspase 1 is an essential component in the development of lupus and its associated vascular dysfunction and that it may play an important role in the cross-talk between environmental exposures and autoimmunity development, thus identifying a novel pathway for therapeutic targeting.

Indexed as

AnimalsAutoantibodiesCaspase 1CytokinesDisease Models, AnimalEndothelium, VascularGlomerulonephritisImmune Complex DiseasesImmunosuppressive AgentsInflammasomesInterferon Type ILupus Erythematosus, SystemicMiceMice, KnockoutTerpenesVascular DiseasesAutoantibodiesCaspase 1CytokinesImmunosuppressive AgentsInflammasomesInterferon Type IpristaneTerpenes

Identifiers

PMID24449582
PMCPMC4135431
OpenAlexW1502316154

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.