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Int J Biol Sci ; 18(1): 331-348, 2022.
Artículo en Inglés | MEDLINE | ID: mdl-34975336

RESUMEN

Pulmonary arterial hypertension (PAH) is characterized by muscularized pulmonary blood vessels, leading to right heart hypertrophy and cardiac failure. However, state-of-the-art therapeutics fail to target the ongoing remodeling process. Here, this study shows that matrix metalloproteinases (MMP)-1 and MMP-10 levels are increased in the medial layer of vessel wall, serum, and M1-polarized macrophages from patients with PAH and the lungs of monocrotaline- and hypoxia-induced PAH rodent models. MMP-10 regulates the malignant phenotype of pulmonary artery smooth muscle cells (PASMCs). The overexpression of active MMP-10 promotes PASMC proliferation and migration via upregulation of cyclin D1 and proliferating cell nuclear antigen, suggesting that MMP-10 produced by infiltrating macrophages contributes to vascular remodeling. Furthermore, inhibition of STAT1 inhibits hypoxia-induced MMP-10 but not MMP-1 expression in M1-polarized macrophages from patients with PAH. In conclusion, circulating MMP-10 could be used as a potential targeted therapy for PAH.


Asunto(s)
Macrófagos/metabolismo , Metaloproteinasa 10 de la Matriz/metabolismo , Metaloproteinasa 1 de la Matriz/metabolismo , Hipertensión Arterial Pulmonar/metabolismo , Remodelación Vascular , Adulto , Anciano , Animales , Movimiento Celular , Proliferación Celular , Modelos Animales de Enfermedad , Femenino , Humanos , Masculino , Persona de Mediana Edad , Miocitos del Músculo Liso/metabolismo , Ratas , Regulación hacia Arriba
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