Alpha2-antiplasmin: A New Target for Fibrotic Diseases

Abstract

Fibrotic diseases are characterized by excessive scarring due to excessive production, deposition, and contraction of the extracellular matrix (ECM). However, the detailed mechanism underlying the development of fibrosis was unclear. Recently, it has been reported that alpha2-antiplasmin (α2AP), which is serine protease inhibitors (serpins), is associated with the development of fibrosis. This review considers the physiological and pathological roles of α2AP in the development of fibrosis, and proposes that α2AP may be a new target for fibrotic disease.

Alpha-2-Antiplasmin : A Fibrinolytic Peptide, could be a Potential Biomarker for Diagnosis of High Altitude Induced Pulmonary Hypertension

“…The key characteristic of PH is pulmonary vascular remodeling, marked by excessive pulmonary vascular smooth muscle cell (PVSMC) proliferation, endothelial medial transformation (EMT) and adventitial differentiation 10,11 . Kanno 12 , reported that α2AP regulates EMT 13,14 . Substantiating the clinical observations, experimental studies in mice deficient in α2AP have shown decreased collagen deposition and diminished myofibroblasts transdifferentiation in vascular injury model 12 .…”

“…Kanno 12 , reported that α2AP regulates EMT 13,14 . Substantiating the clinical observations, experimental studies in mice deficient in α2AP have shown decreased collagen deposition and diminished myofibroblasts transdifferentiation in vascular injury model 12 . Additionally, it was reported that α2AP deficient mice have increased plasmin activity which causes over-release of vascular endothelial growth factor (VEGF) and consequently improved endothelial repair to maintain vascular patency 15 .…”