Evidence map›Paper›PMID 22440612›Full record

ArticleCell metabolism2012

Autophagy links inflammasomes to atherosclerotic progression.

Babak Razani, Chu Feng, Trey Coleman, Roy Emanuel, Haitao Wen, Seungmin Hwang, Jenny P Ting, Herbert W Virgin, Michael B Kastan, Clay F Semenkovich

Open access · bronzeAbstract read
In one paragraph

Article in Cell metabolism, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 336 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
336citing papers in PubMed, 1 pooled it
23.2field-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

336 citing papers in PubMed, 1 synthesis or guideline pooled it, 591 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Theaflavin attenuates atherosclerosis by targeting GSK-3β to suppress pyroptosis and Promote Autophagy in macrophages.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
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  8. From lipid overload to autophagy collapse: how lipid dysregulation drives chronic inflammation and metabolic disease.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
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276 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 3 institutions in 1 country.

Babak RazaniDivision of Endocrinology, Metabolism, and Lipid Research, Department of Medicine, Washington University School of Medicine, St. Louis MO 63110, USA.
Chu Feng
Trey Coleman
Roy Emanuel
Haitao Wen
Seungmin Hwang
Jenny P Ting
Herbert W Virgin
Michael B Kastan
Clay F Semenkovich
Washington University in St. Louis · USUniversity of North Carolina at Chapel Hill · USSt. Jude Children's Research Hospital · US

Funding

Washington University Nutrition Obesity Research CenterP30DK056341 · NIDDK · WASHINGTON UNIVERSITY · PI Brian N Finck · 1999 to 2026
$30.2M
WU P&FP30DK020579 · NIDDK · WASHINGTON UNIVERSITY · PI Irfan J Lodhi · 2013 to 2026
$27.1M
TRANSGENICS COREP60DK020579 · NIDDK · WASHINGTON UNIVERSITY · PI SCHAFFER, JEAN E. · 1986 to 2012
$25.2M
Vascular Surgery and Histopathology CoreP50HL083762 · NHLBI · WASHINGTON UNIVERSITY · PI SEMENKOVICH, CLAY F. · 2006 to 2010
$9.9M
The role of ATM in Metabolic Stress ResponsesR01CA157216 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI KASTAN, MICHAEL B · 2011 to 2020
$3.1M
DE NOVO LIPOGENESIS AND METABOLIC DISEASER01DK076729 · NIDDK · WASHINGTON UNIVERSITY · PI SEMENKOVICH, CLAY F. · 2007 to 2015
$2.5M
OBESITY, ADIPOGENESIS, AND LIPID LIGANDSR01DK088083 · NIDDK · WASHINGTON UNIVERSITY · PI SEMENKOVICH, CLAY F. · 2010 to 2013
$1.3M
De Novo Lipogenesis in Myocardial DysfunctionK08HL098559 · NHLBI · WASHINGTON UNIVERSITY · PI RAZANI, BABAK · 2010 to 2014
$589k
NCI NIH HHS R01 CA157216NHLBI NIH HHS 5K08HL098559NHLBI NIH HHS HL083762NHLBI NIH HHS K08 HL098559NHLBI NIH HHS P50 HL083762NIDDK NIH HHS DK076729NIDDK NIH HHS DK088083NIDDK NIH HHS DK20579NIDDK NIH HHS DK56341NIDDK NIH HHS P30 DK020579NIDDK NIH HHS P30 DK056341NIDDK NIH HHS P60 DK020579NIDDK NIH HHS R01 DK076729NIDDK NIH HHS R01 DK088083
6 · The paper itself

Abstract

We investigated the role of autophagy in atherosclerosis. During plaque formation in mice, autophagic markers colocalized predominantly with macrophages (mφ). Atherosclerotic aortas had elevated levels of p62, suggesting that dysfunctional autophagy is characteristic of plaques. To determine whether autophagy directly influences atherogenesis, we characterized Beclin-1 heterozygous-null and mφ-specific ATG5-null (ATG5-mφKO) mice, commonly used models of autophagy haploinsufficiency and deficiency, respectively. Haploinsufficent Beclin-1 mice had no atherosclerotic phenotype, but ATG5-mφKO mice had increased plaques, suggesting an essential role for basal levels of autophagy in atheroprotection. Defective autophagy is associated with proatherogenic inflammasome activation. Classic inflammasome markers were robustly induced in ATG5-null mφ, especially when coincubated with cholesterol crystals. Moreover, cholesterol crystals appear to be increased in ATG5-mφKO plaques, suggesting a potentially vicious cycle of crystal formation and inflammasome activation in autophagy-deficient plaques. These results show that autophagy becomes dysfunctional in atherosclerosis and its deficiency promotes atherosclerosis in part through inflammasome hyperactivation.

Indexed as

AutophagyDisease ProgressionAnimalsApoptosis Regulatory ProteinsAtherosclerosisBeclin-1CholesterolDisease Models, AnimalHaploinsufficiencyHeterozygoteInflammasomesInflammationMacrophage ActivationMacrophagesMiceMice, Inbred C57BLApoptosis Regulatory ProteinsBeclin-1Becn1 protein, mouseCholesterolInflammasomes

Identifiers

PMID22440612
PMCPMC3322320
OpenAlexW1988747541

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.