Molecular Mechanisms of ADAMTS7 in the Pathogenesis of Ischemic Heart Disease: A Narrative Review

Abstract

Ischemic heart disease (IHD) remains one of the leading global causes of death, primarily driven by atherosclerotic plaque progression and vascular dysfunction. Growing genomic and molecular evidence identifies A Disintegrin and Metalloproteinase with Thrombospondin Motifs-7 (ADAMTS7) as a key mediator in these pathological processes. ADAMTS7, a secreted zinc-dependent metalloproteinase, contributes to vascular smooth muscle cell migration by degrading extracellular matrix components such as cartilage oligomeric matrix protein (COMP). Several single-nucleotide polymorphisms, including the widely studied rs3825807 variant, have been associated with increased susceptibility to IHD, highlighting the genetic relevance of ADAMTS7. This narrative review synthesizes current literature on the genetic associations, molecular mechanisms, regulatory pathways, and translational implications of ADAMTS7 in ischemic heart disease. It further explores its emerging value as a biomarker and its potential as a therapeutic target for cardiovascular disease prevention and management.