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    Antioxidant Activity Mediates Pirfenidone Antifibrotic Effects in Human Pulmonary Vascular Smooth Muscle Cells Exposed to Sera of Idiopathic Pulmonary Fibrosis Patients.

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    IPF Paper.pdf (1.643Mb)
    Date
    2018-10-21
    Author
    Fois, Alessandro Giuseppe
    Posadino, Anna Maria
    Giordo, Roberta
    Cossu, Annalisa
    Agouni, Abdelali
    Rizk, Nasser Moustafa
    Pirina, Pietro
    Carru, Ciriaco
    Zinellu, Angelo
    Pintus, Gianfranco
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    Abstract
    Idiopathic pulmonary fibrosis (IPF) is a chronic lung disease characterized by an exacerbated fibrotic response. Although molecular and cellular determinants involved in the onset and progression of this devastating disease are largely unknown, an aberrant remodeling of the pulmonary vasculature appears to have implications in IPF pathogenesis. Here, we demonstrated for the first time that an increase of reactive oxygen species (ROS) generation induced by sera from IPF patients drives both collagen type I deposition and proliferation of primary human pulmonary artery smooth muscle cells (HPASMCs). IPF sera-induced cellular effects were significantly blunted in cells exposed to the NADPH oxidase inhibitor diphenyleneiodonium (DPI) proving the causative role of ROS and suggesting their potential cellular source. Contrary to IPF naive patients, sera from Pirfenidone-treated IPF patients failed to significantly induce both ROS generation and collagen synthesis in HPASMCs, mechanistically implicating antioxidant properties as the basis for the in vivo effect of this drug.
    DOI/handle
    http://dx.doi.org/10.1155/2018/2639081
    http://hdl.handle.net/10576/11182
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    • Biomedical Sciences [‎268 ‎ items ]
    • Biomedical Research Center Research [‎287 ‎ items ]

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