ADAMTS7: a Novel Therapeutic Target in Atherosclerosis.

Autor: Chung A; Cardiometabolic Genomics Program, Division of Cardiology, Department of Medicine, Columbia University, New York, NY, USA., Reilly MP; Cardiometabolic Genomics Program, Division of Cardiology, Department of Medicine, Columbia University, New York, NY, USA.; Irving Institute for Clinical and Translational Research, Columbia University, New York, NY, USA., Bauer RC; Cardiometabolic Genomics Program, Division of Cardiology, Department of Medicine, Columbia University, New York, NY, USA. rcb36@columbia.edu.
Jazyk: angličtina
Zdroj: Current atherosclerosis reports [Curr Atheroscler Rep] 2023 Aug; Vol. 25 (8), pp. 447-455. Date of Electronic Publication: 2023 Jun 24.
DOI: 10.1007/s11883-023-01115-0
Abstrakt: Purpose of Review: Genome-wide association studies have repeatedly linked the metalloproteinase ADAMTS7 to coronary artery disease. Here we aim to highlight recent findings surrounding the human genetics of ADAMTS7, novel mouse models that investigate ADAMTS7 function, and potential substrates of ADAMTS7 cleavage.
Recent Findings: Recent genome-wide association studies in coronary artery disease have replicated the GWAS signal for ADAMTS7 and shown that the signal holds true even across different ethnic groups. However, the direction of effect in humans remains unclear. A recent novel mouse model revealed that the proatherogenicity of ADAMTS7 is derived from its catalytic functions, while at the translational level, vaccinating mice against ADAMTS7 reduced atherosclerosis. Finally, in vitro proteomics approaches have identified extracellular matrix proteins as candidate substrates that may be causal for the proatherogenicity of ADAMTS7. ADAMTS7 represents an enticing target for therapeutic intervention. The recent studies highlighted here have replicated prior findings, confirming the genetic link between ADAMTS7 and atherosclerosis, while providing further evidence in mice that ADAMTS7 is a targetable proatherogenic enzyme.
(© 2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)
Databáze: MEDLINE
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