Unchecked thrombin is bad news for troubled arteries.
Thrombin is clearly a key trigger of thrombosis, the proximal cause of most morbidity and mortality in atherosclerotic cardiovascular disease. Might thrombin also contribute to longer-term, structural changes in the arterial wall that promote narrowing and clotting? A study in this issue of the JCI argues that it can. Aihara et al. report 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).
Camerer
Eric
E
Cardiovascular Research Institute, UCSF, San Francisco, California 94158-2517, USA. eric.camerer@ucsf.edu
D000818:Animals; D001158:Arteries / Q000473:pathology / Q000503:physiopathology*; D004195:Disease Models, Animal; D015844:Heparin Cofactor II / Q000172:deficiency / Q000235:genetics; D006579:Heterozygote; D006801:Humans; D051379:Mice; D018345:Mice, Knockout; D008955:Models, Cardiovascular; D013917:Thrombin / Q000502:physiology*; D013927:Thrombosis / Q000209:etiology / Q000235:genetics / Q000503:physiopathology
D015844:Heparin Cofactor II; D013917:Thrombin