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The Role of Fibrinolytic Regulators in Vascular Dysfunction of Systemic Sclerosis

Department of Clinical Pathological Biochemistry, Faculty of Pharmaceutical Science, Doshisha Women’s College of Liberal Arts, 97-1 Kodo Kyo-tanabe, Kyoto 610-0395, Japan
Int. J. Mol. Sci. 2019, 20(3), 619;
Received: 19 November 2018 / Revised: 28 January 2019 / Accepted: 29 January 2019 / Published: 31 January 2019
(This article belongs to the Special Issue Endothelial Dysfunction: Pathophysiology and Molecular Mechanisms)
Systemic sclerosis (SSc) is a connective tissue disease of autoimmune origin characterized by vascular dysfunction and extensive fibrosis of the skin and visceral organs. Vascular dysfunction is caused by endothelial cell (EC) apoptosis, defective angiogenesis, defective vasculogenesis, endothelial-to-mesenchymal transition (EndoMT), and coagulation abnormalities, and exacerbates the disease. Fibrinolytic regulators, such as plasminogen (Plg), plasmin, α2-antiplasmin (α2AP), tissue-type plasminogen activator (tPA), urokinase-type plasminogen activator (uPA) and its receptor (uPAR), plasminogen activator inhibitor 1 (PAI-1), and angiostatin, are considered to play an important role in the maintenance of endothelial homeostasis, and are associated with the endothelial dysfunction of SSc. This review considers the roles of fibrinolytic factors in vascular dysfunction of SSc. View Full-Text
Keywords: Fibrinolytic regulators; SSc; vascular dysfunction Fibrinolytic regulators; SSc; vascular dysfunction
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Kanno, Y. The Role of Fibrinolytic Regulators in Vascular Dysfunction of Systemic Sclerosis. Int. J. Mol. Sci. 2019, 20, 619.

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