Evidence map›Paper›PMID 27549026›Full record

ReviewNature reviews. Rheumatology2016

The inflammatory role of phagocyte apoptotic pathways in rheumatic diseases.

Carla M Cuda, Richard M Pope, Harris Perlman

Open access · greenAbstract readReview
In one paragraph

Review in Nature reviews. Rheumatology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 2 pooled it
5.0field-weighted citation impact, top 4% 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

39 citing papers in PubMed, 2 syntheses or guidelines pooled it, 67 citations in OpenAlex.

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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 at 1 institution in 1 country.

Carla M CudaNorthwestern University, Feinberg School of Medicine, Department of Medicine, Division of Rheumatology, 240 East Huron Street, Chicago, Illinois 60611, USA.
Richard M PopeNorthwestern University, Feinberg School of Medicine, Department of Medicine, Division of Rheumatology, 240 East Huron Street, Chicago, Illinois 60611, USA.
Harris PerlmanNorthwestern University, Feinberg School of Medicine, Department of Medicine, Division of Rheumatology, 240 East Huron Street, Chicago, Illinois 60611, USA.
Northwestern University · US

Funding

Small Animal Surgery and HistologyP01HL108795 · NHLBI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI LOSORDO, DOUGLAS W · 2011 to 2015
$10.7M
Therapeutic Role for P21 in Suppressing IL-1 Beta Mediated PathologiesR01AR050250 · NIAMS · SAINT LOUIS UNIVERSITY · PI PERLMAN, HARRIS R · 2003 to 2014
$3.0M
Role of BH3-Domain Proteins in the Effector Phase of RAR01AR054796 · NIAMS · SAINT LOUIS UNIVERSITY · PI PERLMAN, HARRIS R · 2008 to 2012
$1.8M
Development of a Novel RA/Atherosclerosis Mouse ModelR01AR064546 · NIAMS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI PERLMAN, HARRIS R · 2013 to 2017
$1.6M
Caspase 8: A Novel Suppressor of Dendritic Cell-Mediated AutoimmunityK01AR064313 · NIAMS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI CUDA, CARLA M · 2013 to 2017
$597k
RhEumatoid Arthritis SynOvial tissue Network (REASON)UH2AR067687 · NIAMS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI PERLMAN, HARRIS R, POPE, RICHARD M. · 2014 to 2015
$544k
A novel and improved mouse system for studying macrophage specific gene deletionR21AI092490 · NIAID · NORTHWESTERN UNIVERSITY AT CHICAGO · PI PERLMAN, HARRIS R, STEHLIK, CHRISTIAN · 2011 to 2012
$419k
Role of CCR7 in Clinical Response in Inflammatory ArthritisR21AR065076 · NIAMS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI POPE, RICHARD M. · 2013 to 2014
$361k
NHLBI NIH HHS P01 HL108795NIAID NIH HHS R21 AI092490NIAMS NIH HHS K01 AR064313NIAMS NIH HHS R01 AR050250NIAMS NIH HHS R01 AR054796NIAMS NIH HHS R01 AR064546NIAMS NIH HHS R21 AR065076NIAMS NIH HHS UH2 AR067687
6 · The paper itself

Abstract

Rheumatoid arthritis affects nearly 1% of the world's population and is a debilitating autoimmune condition that can result in joint destruction. During the past decade, inflammatory functions have been described for signalling molecules classically involved in apoptotic and non-apoptotic death pathways, including, but not limited to, Toll-like receptor signalling, inflammasome activation, cytokine production, macrophage polarization and antigen citrullination. In light of these remarkable advances in the understanding of inflammatory mechanisms of the death machinery, this Review provides a snapshot of the available evidence implicating death pathways, especially within the phagocyte populations of the innate immune system, in the perpetuation of rheumatoid arthritis and other rheumatic diseases. Elevated levels of signalling mediators of both extrinsic and intrinsic apoptosis, as well as the autophagy, are observed in the joints of patients with rheumatoid arthritis. Furthermore, risk polymorphisms are present in signalling molecules of the extrinsic apoptotic and autophagy death pathways. Although research into the mechanisms underlying these pathways has made considerable progress, this Review highlights areas where further investigation is particularly needed. This exploration is critical, as new discoveries in this field could lead to the development of novel therapies for rheumatoid arthritis and other rheumatic diseases.

Indexed as

Signal TransductionAnimalsApoptosisApoptosis Regulatory ProteinsAutophagyCASP8 and FADD-Like Apoptosis Regulating ProteinCaspase 8Dendritic CellsFas-Associated Death Domain Proteinfas ReceptorHumansMacrophagesPhagocytesPhagocytosisRheumatic DiseasesApoptosis Regulatory ProteinsCASP8 and FADD-Like Apoptosis Regulating ProteinCaspase 8Fadd protein, mouseFas-Associated Death Domain ProteinFas protein, mousefas Receptor

Identifiers

PMID27549026
PMCPMC5297631
OpenAlexW2509023402

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.