An update on factor XII-driven vascular inflammation

Reiner K Mailer; Chandini Rangaswamy; Sandra Konrath; Jonas Emsley; Thomas Renné

doi:10.1016/j.bbamcr.2021.119166

An update on factor XII-driven vascular inflammation

Standard

An update on factor XII-driven vascular inflammation. / Mailer, Reiner K; Rangaswamy, Chandini; Konrath, Sandra; Emsley, Jonas; Renné, Thomas.

in: BBA-MOL CELL RES, Jahrgang 1869, Nr. 1, 119166, 01.2022.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Review › Forschung

Harvard

Mailer, RK, Rangaswamy, C, Konrath, S, Emsley, J & Renné, T 2022, 'An update on factor XII-driven vascular inflammation', BBA-MOL CELL RES, Jg. 1869, Nr. 1, 119166. https://doi.org/10.1016/j.bbamcr.2021.119166

APA

Mailer, R. K., Rangaswamy, C., Konrath, S., Emsley, J., & Renné, T. (2022). An update on factor XII-driven vascular inflammation. BBA-MOL CELL RES, 1869(1), [119166]. https://doi.org/10.1016/j.bbamcr.2021.119166

Vancouver

Mailer RK, Rangaswamy C, Konrath S, Emsley J, Renné T. An update on factor XII-driven vascular inflammation. BBA-MOL CELL RES. 2022 Jan;1869(1). 119166. https://doi.org/10.1016/j.bbamcr.2021.119166

Bibtex

@article{967aff20bbad460badff45020a5b54d1,

title = "An update on factor XII-driven vascular inflammation",

abstract = "The plasma protein factor XII (FXII) is the liver-derived zymogen of the serine protease FXIIa that initiates an array of proteolytic cascades. Zymogen activation, enzymatic FXIIa activity and functions are regulated by interactions with cell receptors, negatively charged surfaces, other serine proteases, and serpin inhibitors, which bind to distinct protein domains and regions in FXII(a). FXII exerts mitogenic activity, while FXIIa initiates the pro-inflammatory kallikrein-kinin pathway and the pro-thrombotic intrinsic coagulation pathway, respectively. Growing evidence indicates that FXIIa-mediated thrombo-inflammation plays a crucial role in various pathological states besides classical thrombosis, such as endothelial dysfunction. Consistently, increased FXIIa levels are associated with hypercholesterolemia and hypertriglyceridemia. In contrast, FXII deficiency protects from thrombosis but is otherwise not associated with prolonged bleeding or other adverse clinical manifestations. Here, we review current concepts for FXII(a)-driven vascular inflammation focusing on endothelial hyperpermeability, receptor signaling, atherosclerosis and immune cell activation.",

keywords = "Angioedema/metabolism, Animals, Atherosclerosis/metabolism, Endothelium, Vascular/metabolism, Factor XII/genetics, Factor XII Deficiency/metabolism, Humans, Inflammation",

author = "Mailer, {Reiner K} and Chandini Rangaswamy and Sandra Konrath and Jonas Emsley and Thomas Renn{\'e}",

year = "2022",

month = jan,

doi = "10.1016/j.bbamcr.2021.119166",

language = "English",

volume = "1869",

journal = "BBA-MOL CELL RES",

issn = "0167-4889",

publisher = "Elsevier",

number = "1",

}

RIS

TY - JOUR

T1 - An update on factor XII-driven vascular inflammation

AU - Mailer, Reiner K

AU - Rangaswamy, Chandini

AU - Konrath, Sandra

AU - Emsley, Jonas

AU - Renné, Thomas

PY - 2022/1

Y1 - 2022/1

N2 - The plasma protein factor XII (FXII) is the liver-derived zymogen of the serine protease FXIIa that initiates an array of proteolytic cascades. Zymogen activation, enzymatic FXIIa activity and functions are regulated by interactions with cell receptors, negatively charged surfaces, other serine proteases, and serpin inhibitors, which bind to distinct protein domains and regions in FXII(a). FXII exerts mitogenic activity, while FXIIa initiates the pro-inflammatory kallikrein-kinin pathway and the pro-thrombotic intrinsic coagulation pathway, respectively. Growing evidence indicates that FXIIa-mediated thrombo-inflammation plays a crucial role in various pathological states besides classical thrombosis, such as endothelial dysfunction. Consistently, increased FXIIa levels are associated with hypercholesterolemia and hypertriglyceridemia. In contrast, FXII deficiency protects from thrombosis but is otherwise not associated with prolonged bleeding or other adverse clinical manifestations. Here, we review current concepts for FXII(a)-driven vascular inflammation focusing on endothelial hyperpermeability, receptor signaling, atherosclerosis and immune cell activation.

AB - The plasma protein factor XII (FXII) is the liver-derived zymogen of the serine protease FXIIa that initiates an array of proteolytic cascades. Zymogen activation, enzymatic FXIIa activity and functions are regulated by interactions with cell receptors, negatively charged surfaces, other serine proteases, and serpin inhibitors, which bind to distinct protein domains and regions in FXII(a). FXII exerts mitogenic activity, while FXIIa initiates the pro-inflammatory kallikrein-kinin pathway and the pro-thrombotic intrinsic coagulation pathway, respectively. Growing evidence indicates that FXIIa-mediated thrombo-inflammation plays a crucial role in various pathological states besides classical thrombosis, such as endothelial dysfunction. Consistently, increased FXIIa levels are associated with hypercholesterolemia and hypertriglyceridemia. In contrast, FXII deficiency protects from thrombosis but is otherwise not associated with prolonged bleeding or other adverse clinical manifestations. Here, we review current concepts for FXII(a)-driven vascular inflammation focusing on endothelial hyperpermeability, receptor signaling, atherosclerosis and immune cell activation.

KW - Angioedema/metabolism

KW - Animals

KW - Atherosclerosis/metabolism

KW - Endothelium, Vascular/metabolism

KW - Factor XII/genetics

KW - Factor XII Deficiency/metabolism

KW - Humans

KW - Inflammation

U2 - 10.1016/j.bbamcr.2021.119166

DO - 10.1016/j.bbamcr.2021.119166

M3 - SCORING: Review article

C2 - 34699874

VL - 1869

JO - BBA-MOL CELL RES

JF - BBA-MOL CELL RES

SN - 0167-4889

IS - 1

M1 - 119166

ER -