Evidence map›Paper›PMID 25036095›Full record

ReviewCurrent opinion in rheumatology2014

Beyond apoptosis in lupus.

Lucrezia Colonna, Christian Lood, Keith B Elkon

Abstract readReview
In one paragraph

Review in Current opinion in rheumatology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 1 pooled it
–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

43 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  8. Article
  9. Multiple Roles of the Stress Sensor GCN2 in Immune Cells.International journal of molecular sciences · 2023
    Review
  10. The role of mitochondria in rheumatic diseases.Nature reviews. Rheumatology · 2022
    Review
  11. Article
  12. Review
  13. 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

3 authors.

Lucrezia ColonnaDivision of Rheumatology, University of Washington, Seattle, Washington, USA *Lucrezia Colonna and Christian Lood contributed equally to the writing of this article.
Christian Lood
Keith B Elkon

Funding

Agonists and Antagonists of Neuropsychiatric LupusR01NS065933 · NINDS · UNIVERSITY OF WASHINGTON · PI ELKON, KEITH B. · 2009 to 2012
$1.4M
Investigating the molecular mechanisms underlying lupus susceptibility conferredF32AR065837 · NIAMS · UNIVERSITY OF WASHINGTON · PI COLONNA, LUCREZIA · 2014 to 2014
$55k
NIAMS NIH HHS 1 F32 AR065837-01NIAMS NIH HHS F32 AR065837NINDS NIH HHS R01 NS065933
6 · The paper itself

Abstract

purpose of reviewSystemic lupus erythematosus (SLE) is characterized by autoantibodies directed against nuclear autoantigens normally concealed from immune recognition in healthy individuals. Here, we summarize recently identified mechanisms of abnormal cell death leading to exposure and aberrant processing of nucleoprotein self antigens, and discuss their role in the SLE pathogenesis. RECENT

findingsDuring the past few years, the unveiling of several new forms of cell death has expanded our understanding beyond the simple view of 'apoptotic' versus 'necrotic' cell death. SLE patients show abnormalities in cell death at several levels, including increased rates of apoptosis, necrosis, and autophagy, as well as reduced clearance of dying cells. These abnormalities lead to an increased autoantigen burden and antigen modifications, such as nucleic acid oxidation that increases the inflammatory properties of self antigens. Recent investigations have highlighted the role of opsonins in determining the immunogenic versus tolerogenic characteristics of self antigens. SUMMARY: Dysregulation of different forms of programmed cell death contributes to increased exposure, availability, and immunogenic characteristics of intracellular self antigens, which all participate in development of lupus autoimmunity. As our understanding of abnormalities of cell death in SLE advances, potential therapeutic opportunities await human implementation.

Indexed as

ApoptosisAutophagyCell DeathHumansLupus Erythematosus, SystemicMicroRNAsModels, BiologicalNecrosisOpsonin ProteinsReceptors, Cell SurfaceMicroRNAsOpsonin ProteinsReceptors, Cell Surface

Identifiers

PMID25036095
PMCPMC4272326

What OpenQuestion holds

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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.