Abstract
Extracellular matrix metalloproteinase ADAMTS1 (adhesion metalloproteinase with thrombospondin-type domain 1) is a key regulator in cardiovascular remodeling with functional paradoxes. This review synthesizes existing evidence to clarify its context-dependent dual roles across various cardiovascular diseases: on the one hand, ADAMTS1 exerts protective functions by maintaining vascular integrity and mitigating inflammatory responses; on the other hand, in conditions such as myocardial infarction and aortic aneurysms, ADAMTS1 promotes pathological progression by excessively hydrolyzing the multifunctional proteoglycan versican and other substrates, leading to tissue disruption and adverse remodeling. This functional switch in ADAMTS1 is jointly regulated by its cellular origin, temporal expression dynamics, and local microenvironment. In summary, ADAMTS1 represents a critical homeostasis node in the cardiovascular system. Therapeutic interventions targeting it should avoid broad-spectrum inhibition strategies; instead, future efforts should focus on developing precise, context-specific regulatory approaches.