Evidence map›Paper›PMID 9691094›Full record

ArticleThe Journal of clinical investigation1998

Expression of the elastolytic cathepsins S and K in human atheroma and regulation of their production in smooth muscle cells.

G K Sukhova, G P Shi, D I Simon, H A Chapman, P Libby

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 209 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
209citing papers in PubMed, 1 pooled it
8.5field-weighted citation impact, top 2% 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

209 citing papers in PubMed, 1 synthesis or guideline pooled it, 669 citations in OpenAlex.

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  13. Circulating protein biomarkers and their association with vulnerable plaque characteristics - a PROSPECT II substudy.International journal of cardiology. Cardiovascular risk and prevention · 2025
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149 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

5 authors at 2 institutions in 1 country.

G K SukhovaBrigham and Women's Hospital, Vascular Medicine and Atherosclerosis Unit and Cardiovascular and Respiratory Divisions, Department of Medicine, Boston, Massachusetts 02115, USA.
G P Shi
D I Simon
H A Chapman
P Libby
Harvard University Press · USRecycled Materials Resource Center · US

Funding

Inflammation in Vascular Injury and RepairR37HL057506 · NHLBI · CASE WESTERN RESERVE UNIVERSITY · PI SIMON, DANIEL I · 2007 to 2016
$4.1M
HUMAN ALVEOLAR MACROPHAGE ELASTASES IN EMPHYSEMAR01HL048261 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI CHAPMAN, HAROLD A · 1993 to 2007
$2.5M
Inflammation in Vascular Injury and RepairR01HL057506 · NHLBI · CASE WESTERN RESERVE UNIVERSITY · PI SIMON, DANIEL I · 1997 to 2006
$2.4M
Inflammatory Mechanisms of AtherosclerosisR01HL034636 · NHLBI · TUFTS UNIVERSITY BOSTON · PI LIBBY, PETER · 1985 to 2006
$1.9M
CONTROL OF GROWTH OF VASCULAR WALL CELLSR37HL034636 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI LIBBY, PETER · 1993 to 2002
$1.2M
NHLBI NIH HHS HL-34636NHLBI NIH HHS HL-48261NHLBI NIH HHS HL/DK-57506
6 · The paper itself

Abstract

Formation of the atherosclerotic intima must involve altered metabolism of the elastin-rich arterial extracellular matrix. Proteases potentially involved in these processes remain unclear. This study examined the expression of the potent elastases cathepsins S and K in human atheroma. Normal arteries contained little or no cathepsin K or S. In contrast, macrophages in atheroma contained abundant immunoreactive cathepsins K and S. Intimal smooth muscle cells (SMC), especially cells appearing to traverse the internal elastic laminae, also contained these enzymes. Extracts of atheromatous tissues had approximately twofold greater elastase-specific activity than extracts of uninvolved arteries, mostly due to cysteine proteases. Cultured human SMC displayed no immunoreactive cathepsins K and S and exhibited little or no elastolytic activity when incubated with insoluble elastin. SMC stimulated with the atheroma-associated cytokines IL-1beta or IFN-gamma secreted active cathepsin S and degraded substantial insoluble elastin (15-20 microg/10(6) cells/24 h). A selective inhibitor of cathepsin S blocked > 80% of this elastolytic activity. The presence of cathepsins K and S at sites of vascular matrix remodeling and the ability of SMC and macrophages to use these enzymes to degrade elastin supports a role for elastolytic cathepsins in vessel wall remodeling and identifies novel therapeutic targets in regulating plaque stability.

Indexed as

ArteriosclerosisCarotid StenosisCathepsin KCathepsinsCells, CulturedCoronary DiseaseElastinEnzyme InductionHumansInterferon-gammaMuscle, Smooth, VascularRNA, MessengerTunica IntimaCathepsin Kcathepsin SCathepsinsCTSK protein, humanElastinInterferon-gammaRNA, Messenger

Identifiers

PMID9691094
PMCPMC508918
OpenAlexW1994641823

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.