statement that haploinsufficiency of heparin cofactor II, a glycosaminoglycan-dependent thrombin inhibitor, exacerbates injury- or hyperlipidemia-induced arterial lesion formation in mice, possibly by excessive thrombin signaling through protease-activated receptors (see the related article beginning on page 1514)

statement that haploinsufficiency of heparin cofactor II, a glycosaminoglycan-dependent thrombin inhibitor, exacerbates injury- or hyperlipidemia-induced arterial lesion formation in mice,…