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Norway

PMID:25712208  

ADAMTS-7 inhibits re-endothelialization of injured arteries and promotes vascular remodeling through cleavage of thrombospondin-1.

Thorsten Kessler | Lu Zhang | Ziyi Liu | Xiaoke Yin | Yaqian Huang | Yingbao Wang | Yi Fu | Manuel Mayr | Qing Ge | Qingbo Xu | Yi Zhu | Xian Wang | Kjestine Schmidt | Cor de Wit | Jeanette Erdmann | Heribert Schunkert | Zouhair Aherrahrou | Wei Kong
Circulation | 2015

ADAMTS-7, a member of the disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS) family, was recently identified to be significantly associated genomewide with coronary artery disease. However, the mechanisms that link ADAMTS-7 and coronary artery disease risk remain elusive. We have previously demonstrated that ADAMTS-7 promotes vascular smooth muscle cell migration and postinjury neointima formation via degradation of a matrix protein cartilage oligomeric matrix protein. Because delayed endothelium repair renders neointima and atherosclerosis plaque formation after vessel injury, we examined whether ADAMTS-7 also inhibits re-endothelialization.

Pubmed ID: 25712208

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Associated grants

  • Agency: British Heart Foundation, United Kingdom
    Id: FS/13/2/29892

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International Mouse Phenotyping Consortium (IMPC) (tool)

RRID:SCR_006158

Center that produces knockout mice and carries out high-throughput phenotyping of each line in order to determine function of every gene in mouse genome. These mice will be preserved in repositories and made available to scientific community representing valuable resource for basic scientific research as well as generating new models for human diseases.

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