Evidence map›Paper›PMID 28987865›Full record

ArticleMatrix biology : journal of the International Society for Matrix Biology2018

Hyaluronan synthase 3 promotes plaque inflammation and atheroprogression.

Susanne Homann, Maria Grandoch, Lena S Kiene, Yanina Podsvyadek, Kathrin Feldmann, Berit Rabausch, Nadine Nagy, Stefan Lehr, Inga Kretschmer, Alexander Oberhuber and 2 more

Open access · greenAbstract read
In one paragraph

Article in Matrix biology : journal of the International Society for Matrix Biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

27 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
  2. Review
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  4. Article
  5. Hyaluronan in cardiac disease: implications for the extracellular matrix beyond collagen.American journal of physiology. Heart and circulatory physiology · 2026
    Review
  6. Article
  7. Review
  8. Article
  9. Article
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  12. TSG6 hyaluronan matrix remodeling dampens the inflammatory response during colitis.Matrix biology : journal of the International Society for Matrix Biology · 2023
    Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Reduction ofFrontiers in cardiovascular medicine · 2022
    Article
  19. Article
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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

12 authors at 3 institutions in 2 countries.

Susanne HomannInstitut für Pharmakologie und Klinische Pharmakologie, University Hospital, Heinrich-Heine-University Düsseldorf, Düsseldorf, Germany.
Maria GrandochInstitut für Pharmakologie und Klinische Pharmakologie, University Hospital, Heinrich-Heine-University Düsseldorf, Düsseldorf, Germany.
Lena S KieneInstitut für Pharmakologie und Klinische Pharmakologie, University Hospital, Heinrich-Heine-University Düsseldorf, Düsseldorf, Germany.
Yanina PodsvyadekInstitut für Pharmakologie und Klinische Pharmakologie, University Hospital, Heinrich-Heine-University Düsseldorf, Düsseldorf, Germany.
Kathrin FeldmannInstitut für Pharmakologie und Klinische Pharmakologie, University Hospital, Heinrich-Heine-University Düsseldorf, Düsseldorf, Germany.
Berit RabauschInstitut für Pharmakologie und Klinische Pharmakologie, University Hospital, Heinrich-Heine-University Düsseldorf, Düsseldorf, Germany.
Nadine NagyInstitut für Pharmakologie und Klinische Pharmakologie, University Hospital, Heinrich-Heine-University Düsseldorf, Düsseldorf, Germany; Division of Infectious Diseases and Geographic Medicine, Department of Medicine, Stanford Immunology, Stanford, USA.
Stefan LehrInstitute of Clinical Biochemistry and Pathobiochemistry, German Diabetes Center at the Heinrich-Heine-University Duesseldorf, Leibniz Center for Diabetes Research, Düsseldorf, Germany.
Inga KretschmerInstitut für Pharmakologie und Klinische Pharmakologie, University Hospital, Heinrich-Heine-University Düsseldorf, Düsseldorf, Germany.
Alexander OberhuberDepartment of Vascular and Endovascular Surgery, University Hospital Düsseldorf, Düsseldorf, Germany.
Paul BollykyDivision of Infectious Diseases and Geographic Medicine, Department of Medicine, Stanford Immunology, Stanford, USA.
Jens W FischerInstitut für Pharmakologie und Klinische Pharmakologie, University Hospital, Heinrich-Heine-University Düsseldorf, Düsseldorf, Germany; CARID, Cardiovascular Research Institute Düsseldorf, University Hospital, Heinrich-Heine-University Düsseldorf, Düsseldorf, Germany. Electronic address: jens.fischer@uni-duesseldorf.de.
Düsseldorf University Hospital · DEDeutsches Diabetes-Zentrum e.V. · DEStanford Medicine · US

Funding

Tissue Cytokine Sequestration and Immune Regulation in AutoimmunityU01AI101984 · NIAID · STANFORD UNIVERSITY · PI BOLLYKY, PAUL L · 2012 to 2021
$5.0M
Lymph Node Extracellular Matrix in Antigen Presentation and Immune RegulationR01DK096087 · NIDDK · STANFORD UNIVERSITY · PI BOLLYKY, PAUL L · 2012 to 2021
$3.4M
ECM Costimulation of Immunoregulatory Pathways in Airway InflammationR01HL113294 · NHLBI · STANFORD UNIVERSITY · PI BOLLYKY, PAUL L · 2012 to 2016
$2.0M
NHLBI NIH HHS R01 HL113294NIAID NIH HHS U01 AI101984NIDDK NIH HHS R01 DK096087
6 · The paper itself

Abstract

objectiveHyaluronan (HA) is a prominent component of the provisional extracellular matrix (ECM) present in the neointima of atherosclerotic plaques. Here the role of HA synthase 3 (HAS3) in atheroprogression was studied. APPROACH AND

resultsIt is demonstrated here that HAS isoenzymes 1, -2 and -3 are expressed in human atherosclerotic plaques of the carotid artery. In Apolipoprotein E (Apoe)-deficient mice Has3 expression is increased early during lesion formation when macrophages enter atherosclerotic plaques. Importantly, HAS3 expression in vascular smooth muscle cells (VSMC) was found to be regulated by interleukin 1 β (IL-1β) in an NFkB dependent manner and blocking antibodies to IL-1β abrogate Has3 expression in VSMC by activated macrophages. Has3/Apoe double deficient mice developed less atherosclerosis characterized by decreased Th1-cell responses, decreased IL-12 release, and decreased macrophage-driven inflammation.

conclusionsInhibition of HAS3-dependent synthesis of HA dampens systemic Th1 cell polarization and reduces plaque inflammation. These data suggest that HAS3 might be a promising therapeutic target in atherosclerosis. Moreover, because HAS3 is regulated by IL-1β, our results suggest that therapeutic anti-IL-1β antibodies, recently tested in human clinical trials (CANTOS), may exert their beneficial effects on inflammation in post-myocardial infarction patients in part via effects on HAS3. TOC categorybasic study TOC subcategoryarteriosclerosis.

Indexed as

AnimalsApolipoproteins ECell PolarityCells, CulturedDisease Models, AnimalDisease ProgressionHumansHyaluronan SynthasesHyaluronic AcidInterleukin-1betaMacrophagesMiceMuscle, Smooth, VascularMyocytes, Smooth MuscleNF-kappa BPlaque, AtheroscleroticApolipoproteins EHAS3 protein, humanHyaluronan SynthasesHyaluronic AcidIL1B protein, humanInterleukin-1betaNF-kappa BAtherosclerosisHyaluronanInflammationInterleukin 1 betaMacrophageT-cellsVascular Biology

Identifiers

PMID28987865
PMCPMC6023397
OpenAlexW2762044378

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.