Evidence map›Paper›PMID 29885460›Full record

ReviewMatrix biology : journal of the International Society for Matrix Biology2018

ADAMTS proteins in human disorders.

Timothy J Mead, Suneel S Apte

Open access · greenAbstract readReview
In one paragraph

Review 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 171 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
171citing papers in PubMed, 3 pooled it
15.7field-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

171 citing papers in PubMed, 3 syntheses or guidelines pooled it, 273 citations in OpenAlex.

  1. Pooled it
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  3. Pooled it
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  8. Review
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  12. Article
  13. Modeling Aspects of Human Placental Development with Trophoblast Stem Cells.Methods in molecular biology (Clifton, N.J.) · 2026
    Article
  14. An Overview of ADAMTS Proteases.Methods in molecular biology (Clifton, N.J.) · 2026
    Review
  15. Article
  16. Article
  17. Article
  18. Generation of a conditionalMatrix biology plus · 2025
    Article
  19. Article
  20. Review

111 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

2 authors at 1 institution in 1 country.

Timothy J MeadDepartment of Biomedical Engineering, Cleveland Clinic Lerner Research Institute, Cleveland, OH 44195, United States.
Suneel S ApteDepartment of Biomedical Engineering, Cleveland Clinic Lerner Research Institute, Cleveland, OH 44195, United States. Electronic address: aptes@ccf.org.
Cleveland Clinic Lerner College of Medicine · US

Funding

Extracellular matrix remodeling in ocular anterior segment developmentR01EY024943 · NEI · CLEVELAND CLINIC LERNER COM-CWRU · PI APTE, SUNEEL S · 2015 to 2017
$1.1M
NEI NIH HHS R01 EY024943
6 · The paper itself

Abstract

ADAMTS proteins are a superfamily of 26 secreted molecules comprising two related, but distinct families. ADAMTS proteases are zinc metalloendopeptidases, most of whose substrates are extracellular matrix (ECM) components, whereas ADAMTS-like proteins lack a metalloprotease domain, reside in the ECM and have regulatory roles vis-à-vis ECM assembly and/or ADAMTS activity. Evolutionary conservation and expansion of ADAMTS proteins in mammals is suggestive of crucial embryologic or physiological roles in humans. Indeed, Mendelian disorders or birth defects resulting from naturally occurring ADAMTS2, ADAMTS3, ADAMTS10, ADAMTS13, ADAMTS17, ADAMTS20, ADAMTSL2 and ADAMTSL4 mutations as well as numerous phenotypes identified in genetically engineered mice have revealed ADAMTS participation in major biological pathways. Important roles have been identified in a few acquired conditions. ADAMTS5 is unequivocally implicated in pathogenesis of osteoarthritis via degradation of aggrecan, a major structural proteoglycan in cartilage. ADAMTS7 is strongly associated with coronary artery disease and promotes atherosclerosis. Autoantibodies to ADAMTS13 lead to a platelet coagulopathy, thrombotic thrombocytopenic purpura, which is similar to that resulting from ADAMTS13 mutations. ADAMTS proteins have numerous potential connections to other human disorders that were identified by genome-wide association studies. Here, we review inherited and acquired human disorders in which ADAMTS proteins participate, and discuss progress and prospects in therapeutics.

Indexed as

MutationADAMTS ProteinsAnimalsCongenital AbnormalitiesCoronary Artery DiseaseExtracellular MatrixGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansMultigene FamilyOsteoarthritisPurpura, Thrombotic ThrombocytopenicADAMTS ProteinsAtherosclerosisExtracellular matrixGenome-wide association studies (GWAS)MetalloproteaseOsteoarthritisProtease

Identifiers

PMID29885460
PMCPMC6146047
OpenAlexW2805257547

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.