Evidence map›Paper›PMID 26260307›Full record

ReviewJournal of internal medicine2015

Inflammation and plaque vulnerability.

G K Hansson, P Libby, I Tabas

Open access · greenAbstract readReview
In one paragraph

Review in Journal of internal medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 421 papers, 7 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
421citing papers in PubMed, 7 pooled it
27.5field-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

421 citing papers in PubMed, 7 syntheses or guidelines pooled it, 777 citations in OpenAlex.

  1. Pooled it
  2. Vascular medicine (London, England) · 2025
    Pooled it
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  11. Review
  12. Myeloid Cell-Specific Deletion of LGR4 Suppresses Atherosclerotic Lesion Formation.Arteriosclerosis, thrombosis, and vascular biology · 2026
    Article
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  17. Review
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361 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

3 authors at 3 institutions in 2 countries.

G K HanssonDepartment of Medicine and Center for Molecular Medicine, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.
P LibbyDivision of Cardiovascular Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
I TabasDepartment of Medicine, Department of Pathology and Cell Biology, and Department of Physiology, Columbia University Medical Center, New York, NY, USA.
Brigham and Women's Hospital · USColumbia University Irving Medical Center · USKarolinska Institutet · SE

Funding

The Unfolded Protein Response in Sterol CytoxicityR01HL075662 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI TABAS, IRA A · 2004 to 2017
$5.6M
Molecular Determinants of Arterial Remodeling in AtherogenesisR01HL080472 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI LIBBY, PETER · 2005 to 2018
$5.0M
Enhancing Inflammation Resolution in Atherosclerosis via Targeted Nanoparticle-Mediated Delivery of BiologicsR01HL127464 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI SHI, JINJUN, TABAS, IRA A · 2016 to 2019
$3.0M
Mechanisms of Defective Efferocytosis in AtherosclerosisR01HL107497 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI TABAS, IRA A · 2012 to 2015
$1.6M
"MerTK Cleavage and Signaling in Atherosclerosis"R01HL132412 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI TABAS, IRA A · 2016 to 2018
$1.5M
NHLBI NIH HHS HHSN268201000045CNHLBI NIH HHS HL075662NHLBI NIH HHS HL107497NHLBI NIH HHS R01 HL075662NHLBI NIH HHS R01 HL080472NHLBI NIH HHS R01 HL107497NHLBI NIH HHS R01 HL127464NHLBI NIH HHS R01 HL132412PHS HHS HHSN268201000045C
6 · The paper itself

Abstract

Atherosclerosis is a maladaptive, nonresolving chronic inflammatory disease that occurs at sites of blood flow disturbance. The disease usually remains silent until a breakdown of integrity at the arterial surface triggers the formation of a thrombus. By occluding the lumen, the thrombus or emboli detaching from it elicits ischaemic symptoms that may be life-threatening. Two types of surface damage can cause atherothrombosis: plaque rupture and endothelial erosion. Plaque rupture is thought to be caused by loss of mechanical stability, often due to reduced tensile strength of the collagen cap surrounding the plaque. Therefore, plaques with reduced collagen content are thought to be more vulnerable than those with a thick collagen cap. Endothelial erosion, on the other hand, may occur after injurious insults to the endothelium instigated by metabolic disturbance or immune insults. This review discusses the molecular mechanisms involved in plaque vulnerability and the development of atherothrombosis.

Indexed as

Endothelium, VascularPlaque, AtheroscleroticAnimalsCysteine ProteasesHumansInflammationMatrix MetalloproteinasesRupture, SpontaneousThromboembolismCysteine ProteasesMatrix Metalloproteinasesatherosclerosisatherothrombosisen-dothelial erosioninflammationplaque rupture

Identifiers

PMID26260307
PMCPMC5082111
OpenAlexW2150795824

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.