By cleaving TFPI-2, ADAMTS1 indirectly alters the proteolytic environment around cells, potentially disrupting homeostatic balance in atherosclerosis and cancer; (2) Interaction with Syndecan-4: ADAMTS1 participates in the shedding of Syndecan-4 (multiligand proteoglycan-4)—a process that, while promoting immune cell recruitment, paradoxically alleviates cardiac dysfunction in lipopolysaccharide (LPS)-induced inflammation [57]. Here, ADAMTS1 is linked to atherosclerosis.