Evidence map›Paper›PMID 23307734›Full record

ReviewScience (New York, N.Y.)2013

Anti-inflammatory therapy in chronic disease: challenges and opportunities.

Ira Tabas, Christopher K Glass

Abstract readReview
In one paragraph

Review in Science (New York, N.Y.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 534 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
534citing papers in PubMed, 3 pooled it
46.3field-weighted citation impact, top 1% 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

534 citing papers in PubMed, 3 syntheses or guidelines pooled it, 1,064 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Trial
  5. Lipoxins modulate neutrophil oxidative burst, integrin expression and lymphatic transmigration differentially in human health and atherosclerosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022
    Trial
  6. Altered tissue specialized pro-resolving mediators in chronic rhinosinusitis.Prostaglandins, leukotrienes, and essential fatty acids · 2021
    Trial
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474 more citing papers are in PubMed but not listed here.

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

2 authors at 2 institutions in 1 country.

Ira TabasDepartment of Medicine, Columbia University, New York, NY 10032, USA. iat1@columbia.edu
Christopher K Glass
Columbia University · USUniversity of California San Diego · US

Funding

TTC39B in obesity and atherosclerosisP01HL087123 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI TALL, ALAN RICHARD · 2007 to 2022
$31.2M
Regulation and function of plasma lipid transfer proteinsP01HL054591 · NHLBI · ROCKEFELLER UNIVERSITY · PI GOLDBERG, IRA J · 1995 to 2010
$19.9M
Transcriptional Genomics CoreP01DK074868 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GLASS, CHRISTOPHER K · 2007 to 2016
$16.6M
Transcriptional co-regulators and macrophage gene expressionR01DK091183 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GLASS, CHRISTOPHER K · 2011 to 2025
$9.9M
The Unfolded Protein Response in Sterol CytoxicityR01HL075662 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI TABAS, IRA A · 2004 to 2017
$5.6M
INTERACTION OF ATHEROGENIC LIPOPROTEINS WITH MACROPHAGESR01HL057560 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI TABAS, IRA A · 1997 to 2010
$4.3M
Autophagy in Advanced AtherosclerosisR01HL106019 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI TABAS, IRA A · 2011 to 2014
$1.8M
Mechanisms of Defective Efferocytosis in AtherosclerosisR01HL107497 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI TABAS, IRA A · 2012 to 2015
$1.6M
NHLBI NIH HHS HC088093NHLBI NIH HHS P01 HL054591NHLBI NIH HHS P01-HL054591NHLBI NIH HHS P01 HL087123NHLBI NIH HHS R01 HL057560NHLBI NIH HHS R01-HL057560NHLBI NIH HHS R01 HL075662NHLBI NIH HHS R01-HL075662NHLBI NIH HHS R01 HL106019NHLBI NIH HHS R01 HL107497NIDDK NIH HHS DK074868NIDDK NIH HHS DK091183NIDDK NIH HHS P01 DK074868NIDDK NIH HHS R01 DK091183
6 · The paper itself

Abstract

A number of widespread and devastating chronic diseases, including atherosclerosis, type 2 diabetes, and Alzheimer's disease, have a pathophysiologically important inflammatory component. In these diseases, the precise identity of the inflammatory stimulus is often unknown and, if known, is difficult to remove. Thus, there is interest in therapeutically targeting the inflammatory response. Although there has been success with anti-inflammatory therapy in chronic diseases triggered by primary inflammation dysregulation or autoimmunity, there are considerable limitations. In particular, the inflammatory response is critical for survival. As a result, redundancy, compensatory pathways, and necessity narrow the risk:benefit ratio of anti-inflammatory drugs. However, new advances in understanding inflammatory signaling and its links to resolution pathways, together with new drug development, offer promise in this area of translational biomedical research.

Indexed as

AnimalsAnti-Inflammatory AgentsAutoimmune DiseasesCardiovascular DiseasesChronic DiseaseDiabetes Mellitus, Type 2HumansInflammationNeurodegenerative DiseasesAnti-Inflammatory Agents

Identifiers

PMID23307734
PMCPMC3608517
OpenAlexW2020466729

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.