Evidence map›Paper›PMID 24281248›Full record

ReviewSeminars in immunopathology2014

Impacts of the apoptosis inhibitor of macrophage (AIM) on obesity-associated inflammatory diseases.

Satoko Arai, Toru Miyazaki

Open access · hybridAbstract readReview
In one paragraph

Review in Seminars in immunopathology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.6field-weighted citation impact, top 18% 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, 34 citations in OpenAlex.

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  19. Interaction of AIM with insulin-like growth factor-binding protein-4.International journal of molecular medicine · 2015
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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

2 authors at 2 institutions in 1 country.

Satoko AraiLaboratory of Molecular Biomedicine for Pathogenesis, Center for Disease Biology and Integrative Medicine, Faculty of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-0033, Japan, sarai@m.u-tokyo.ac.jp.
Toru Miyazaki
Japan Science and Technology Agency · JPThe University of Tokyo · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Obesity is associated with various metabolic and cardiovascular diseases caused by chronic, low-grade inflammation that is initially observed in obese adipose tissue. In addition, many etiological studies in humans have shown a strong correlation between obesity and inflammatory autoimmune diseases. In this review, we focus on the involvement of apoptosis inhibitor of macrophage (AIM), a macrophage-derived blood protein, in both types of immune response. Through differential mechanisms, AIM thereby plays key roles in the pathogenesis of atherosclerosis, metabolic diseases, and obesity-associated autoimmune diseases. Thus, the regulation of blood AIM levels or AIM function has the potential to serve as a next-generation therapy against these inflammatory diseases brought about by modern lifestyle.

Indexed as

AdipocytesAdipose TissueAnimalsAutoantibodiesAutoimmunityB-LymphocytesDisease SusceptibilityHumansImmunoglobulin MInflammationInhibitor of Apoptosis ProteinsInsulin ResistanceLipolysisMacrophagesMetabolic SyndromeMiceAutoantibodiesImmunoglobulin MInhibitor of Apoptosis ProteinsPPAR gammaReceptors, FcToll-Like Receptor 4

Identifiers

PMID24281248
PMCPMC3912372
OpenAlexW1971489909

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.