Coagulation factor XII in thrombosis and inflammation

Coen Maas; Thomas Renné

doi:10.1182/blood-2017-04-569111

Coagulation factor XII in thrombosis and inflammation

Standard

Coagulation factor XII in thrombosis and inflammation. / Maas, Coen; Renné, Thomas.

In: BLOOD, Vol. 131, No. 17, 26.04.2018, p. 1903-1909.

Research output: SCORING: Contribution to journal › SCORING: Review article › Research

Harvard

Maas, C & Renné, T 2018, 'Coagulation factor XII in thrombosis and inflammation', BLOOD, vol. 131, no. 17, pp. 1903-1909. https://doi.org/10.1182/blood-2017-04-569111

APA

Maas, C., & Renné, T. (2018). Coagulation factor XII in thrombosis and inflammation. BLOOD, 131(17), 1903-1909. https://doi.org/10.1182/blood-2017-04-569111

Vancouver

Maas C, Renné T. Coagulation factor XII in thrombosis and inflammation. BLOOD. 2018 Apr 26;131(17):1903-1909. https://doi.org/10.1182/blood-2017-04-569111

Bibtex

@article{31885b1b3a2742abb152e0b7e53302de,

title = "Coagulation factor XII in thrombosis and inflammation",

abstract = "Combinations of proinflammatory and procoagulant reactions are the unifying principle for a variety of disorders affecting the cardiovascular system. The factor XII-driven contact system starts coagulation and inflammatory mechanisms via the intrinsic pathway of coagulation and the bradykinin-producing kallikrein-kinin system, respectively. The biochemistry of the contact system in vitro is well understood; however, its in vivo functions are just beginning to emerge. Challenging the concept of the coagulation balance, targeting factor XII or its activator polyphosphate, provides protection from thromboembolic diseases without interfering with hemostasis. This suggests that the polyphosphate/factor XII axis contributes to thrombus formation while being dispensable for hemostatic processes. In contrast to deficiency in factor XII providing safe thromboprotection, excessive FXII activity is associated with the life-threatening inflammatory disorder hereditary angioedema. The current review summarizes recent findings of the polyphosphate/factor XII-driven contact system at the intersection of procoagulant and proinflammatory disease states. Elucidating the contact system offers the exciting opportunity to develop strategies for safe interference with both thrombotic and inflammatory disorders.",

keywords = "Journal Article, Review",

author = "Coen Maas and Thomas Renn{\'e}",

note = "{\textcopyright} 2018 by The American Society of Hematology.",

year = "2018",

month = apr,

day = "26",

doi = "10.1182/blood-2017-04-569111",

language = "English",

volume = "131",

pages = "1903--1909",

journal = "BLOOD",

issn = "0006-4971",

publisher = "American Society of Hematology",

number = "17",

}

RIS

TY - JOUR

T1 - Coagulation factor XII in thrombosis and inflammation

AU - Maas, Coen

AU - Renné, Thomas

PY - 2018/4/26

Y1 - 2018/4/26

N2 - Combinations of proinflammatory and procoagulant reactions are the unifying principle for a variety of disorders affecting the cardiovascular system. The factor XII-driven contact system starts coagulation and inflammatory mechanisms via the intrinsic pathway of coagulation and the bradykinin-producing kallikrein-kinin system, respectively. The biochemistry of the contact system in vitro is well understood; however, its in vivo functions are just beginning to emerge. Challenging the concept of the coagulation balance, targeting factor XII or its activator polyphosphate, provides protection from thromboembolic diseases without interfering with hemostasis. This suggests that the polyphosphate/factor XII axis contributes to thrombus formation while being dispensable for hemostatic processes. In contrast to deficiency in factor XII providing safe thromboprotection, excessive FXII activity is associated with the life-threatening inflammatory disorder hereditary angioedema. The current review summarizes recent findings of the polyphosphate/factor XII-driven contact system at the intersection of procoagulant and proinflammatory disease states. Elucidating the contact system offers the exciting opportunity to develop strategies for safe interference with both thrombotic and inflammatory disorders.

AB - Combinations of proinflammatory and procoagulant reactions are the unifying principle for a variety of disorders affecting the cardiovascular system. The factor XII-driven contact system starts coagulation and inflammatory mechanisms via the intrinsic pathway of coagulation and the bradykinin-producing kallikrein-kinin system, respectively. The biochemistry of the contact system in vitro is well understood; however, its in vivo functions are just beginning to emerge. Challenging the concept of the coagulation balance, targeting factor XII or its activator polyphosphate, provides protection from thromboembolic diseases without interfering with hemostasis. This suggests that the polyphosphate/factor XII axis contributes to thrombus formation while being dispensable for hemostatic processes. In contrast to deficiency in factor XII providing safe thromboprotection, excessive FXII activity is associated with the life-threatening inflammatory disorder hereditary angioedema. The current review summarizes recent findings of the polyphosphate/factor XII-driven contact system at the intersection of procoagulant and proinflammatory disease states. Elucidating the contact system offers the exciting opportunity to develop strategies for safe interference with both thrombotic and inflammatory disorders.

KW - Journal Article

KW - Review

U2 - 10.1182/blood-2017-04-569111

DO - 10.1182/blood-2017-04-569111

M3 - SCORING: Review article

C2 - 29483100

VL - 131

SP - 1903

EP - 1909

JO - BLOOD

JF - BLOOD

SN - 0006-4971

IS - 17

ER -