Evidence map›Paper›PMID 22393536›Full record

ReviewCold Spring Harbor perspectives in medicine2012

Connecting type 1 and type 2 diabetes through innate immunity.

Justin I Odegaard, Ajay Chawla

Open access · bronzeAbstract readReview
In one paragraph

Review in Cold Spring Harbor perspectives in medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers, 9 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
87citing papers in PubMed, 9 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

87 citing papers in PubMed, 9 syntheses or guidelines pooled it, 190 citations in OpenAlex.

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  6. Prevalence of comorbidities and its effects in patients infected with SARS-CoV-2: a systematic review and meta-analysis.International journal of infectious diseases : IJID : official publication of the International Society for Infectious Diseases · 2020
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  8. Prevalence of comorbidities in the Middle East respiratory syndrome coronavirus (MERS-CoV): a systematic review and meta-analysis.International journal of infectious diseases : IJID : official publication of the International Society for Infectious Diseases · 2016
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  17. Intracellular C3 protects β-cells from IL-1β-driven cytotoxicity via interaction with Fyn-related kinase.Proceedings of the National Academy of Sciences of the United States of America · 2024
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27 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.

Justin I OdegaardDepartment of Pathology, Stanford University School of Medicine, Stanford, California 94305, USA.
Ajay Chawla
Stanford University · USUniversity of California, San Francisco · US

Funding

Innate Immune Mechanisms of ThermogenesisR01DK094641 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI WANG, BIAO · 2011 to 2019
$3.5M
Transcriptional Control of Macrophage in AtherogenesisR01HL076746 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI CHAWLA, AJAY · 2004 to 2014
$3.0M
Immune Triggers of Tissue RegenerationDP1OD006415 · OD · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI CHAWLA, AJAY · 2009 to 2011
$2.4M
Nuclear receptor mechanisms controlling macrophage function in health and diseaseR01DK081405 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI CHAWLA, AJAY · 2009 to 2013
$1.8M
Role of Cytokine Signaling Pathways and Macrophages in Type 2 Diabetes MellitusR01DK076760 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI CHAWLA, AJAY · 2007 to 2011
$1.6M
Immune Triggers of Tissue RegenerationDP1AR064158 · NIAMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI CHAWLA, AJAY · 2012 to 2013
$1.5M
NHLBI NIH HHS HL076746NHLBI NIH HHS R01 HL076746NIAMS NIH HHS DP1 AR064158NIDDK NIH HHS DK076760NIDDK NIH HHS R01 DK076760NIDDK NIH HHS R01 DK081405NIDDK NIH HHS R01 DK094641NIH HHS DP1 OD006415
6 · The paper itself

Abstract

The escalating epidemic of obesity has driven the prevalence of both type 1 and 2 diabetes mellitus to historically high levels. Chronic low-grade inflammation, which is present in both type 1 and type 2 diabetics, contributes to the pathogenesis of insulin resistance. The accumulation of activated innate immune cells in metabolic tissues results in release of inflammatory mediators, in particular, IL-1β and TNFα, which promote systemic insulin resistance and β-cell damage. In this article, we discuss the central role of innate immunity and, in particular, the macrophage in insulin sensitivity and resistance, β-cell damage, and autoimmune insulitis. We conclude with a discussion of the therapeutic implications of this integrated understanding of diabetic pathology.

Indexed as

Immunity, InnateAdaptive ImmunityAdipose TissueB-LymphocytesCytokinesDiabetes Mellitus, Type 1Diabetes Mellitus, Type 2HumansInflammasomesInflammationInflammation MediatorsInsulin ResistanceInterleukin-1betaKupffer CellsLiverMacrophagesCytokinesInflammasomesInflammation MediatorsInterleukin-1betaReceptor, InsulinTumor Necrosis Factor-alpha

Identifiers

PMID22393536
PMCPMC3282495
OpenAlexW2137098883

What OpenQuestion holds

Textmetadata
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.