Evidence map›Paper›PMID 20409295›Full record

ArticleBMC cardiovascular disorders2010

Human macrophage foam cells degrade atherosclerotic plaques through cathepsin K mediated processes.

Natasha Barascuk, Helene Skjøt-Arkil, Thomas C Register, Lise Larsen, Inger Byrjalsen, Claus Christiansen, Morten A Karsdal

Open access · goldAbstract read
In one paragraph

Article in BMC cardiovascular disorders, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.1field-weighted citation impact, top 20% 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

21 citing papers in PubMed, 46 citations in OpenAlex.

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  11. Cysteinyl cathepsins in cardiovascular diseases.Biochimica et biophysica acta. Proteins and proteomics · 2020
    Review
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  13. Bone mass density and bone metabolism marker are associated with progression of carotid and cardiac calcified plaque in Chinese elderly population.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2019
    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

7 authors at 2 institutions in 2 countries.

Natasha BarascukNordic Bioscience A/S, Herlev, DK-2730, Denmark. nb@nordicbioscience.com
Helene Skjøt-Arkil
Thomas C Register
Lise Larsen
Inger Byrjalsen
Claus Christiansen
Morten A Karsdal
Nordic Bioscience (Denmark) · DKWake Forest University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundProteolytic degradation of Type I Collagen by proteases may play an important role in remodeling of atherosclerotic plaques, contributing to increased risk of plaque rupture.The aim of the current study was to investigate whether human macrophage foam cells degrade the extracellular matrix (ECM) of atherosclerotic plaques by cathepsin K mediated processes.

methodsWe 1) cultured human macrophages on ECM and measured cathepsin K generated fragments of type I collagen (C-terminal fragments of Type I collagen (CTX-I) 2) investigated the presence of CTX-I in human coronary arteries and 3) finally investigated the clinical potential by measuring circulating CTX-I in women with and without radiographic evidence of aortic calcified atherosclerosis.

resultsImmune-histochemistry of early and advanced lesions of coronary arteries demonstrated co-localization of Cathepsin-K and CTX-I in areas of intimal hyperplasia and in shoulder regions of advanced plaques. Treatment of human monocytes with M-CSF or M-CSF+LDL generated macrophages and foam cells producing CTX-I when cultured on type I collagen enriched matrix. Circulating levels of CTX-I were not significantly different in women with aortic calcifications compared to those without.

conclusionsHuman macrophage foam cells degrade the atherosclerotic plaques though cathepsin K mediated processes, resulting in increase in levels of CTX-I. Serum CTX-I was not elevated in women with aortic calcification, likely due to the contribution of CTX-I from osteoclastic bone resorption which involves Cathepsin-K. The human macrophage model system may be used to identify important pathway leading to excessive proteolytic plaque remodeling and plaque rupture.

Indexed as

AdultAgedCalcinosisCarotid Artery DiseasesCarotid StenosisCathepsin KCells, CulturedCollagen Type IDisease ProgressionExtracellular MatrixFemaleFoam CellsHumansImmunochemistryLipoproteins, LDLMacrophage Colony-Stimulating FactorCathepsin KCollagen Type ILipoproteins, LDLMacrophage Colony-Stimulating FactorPeptide Fragments

Identifiers

PMID20409295
PMCPMC2868786
OpenAlexW2057032262

What OpenQuestion holds

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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.