Cardiac Expression of Factor X Mediates Cardiac Hypertrophy and Fibrosis in Pressure Overload.
JACC Basic Transl Sci
; 5(1): 69-83, 2020 Jan.
Article
en En
| MEDLINE
| ID: mdl-32043021
ABSTRACT
Activated factor X is a key component of the coagulation cascade, but whether it directly regulates pathological cardiac remodeling is unclear. In mice subjected to pressure overload stress, cardiac factor X mRNA expression and activity increased concurrently with cardiac hypertrophy, fibrosis, inflammation and diastolic dysfunction, and responses blocked with a low coagulation-independent dose of rivaroxaban. In vitro, neurohormone stressors increased activated factor X expression in both cardiac myocytes and fibroblasts, resulting in activated factor X-mediated activation of protease-activated receptors and pro-hypertrophic and -fibrotic responses, respectively. Thus, inhibition of cardiac-expressed activated factor X could provide an effective therapy for the prevention of adverse cardiac remodeling in hypertensive patients.
FXa, activated coagulation factor X; HF, heart failure; PAR, protease-activated receptor; PO, pressure-overload; PT, prothrombin time; TAC, transverse aortic constriction; aPTT, activated partial thromboplastin time; activated coagulation factor X; cardiac hypertrophy; coagulation; fibrosis; protease-activated receptors; rivaroxaban
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1
Colección:
01-internacional
Base de datos:
MEDLINE
Idioma:
En
Revista:
JACC Basic Transl Sci
Año:
2020
Tipo del documento:
Article