In a new study, researchers investigated the role of two extracellular Wnt antagonists, secreted frizzled-related protein-1 (SFRP1) and frizzled-related protein (FRZB) in lung fibrosis using in vitro and in vivo models.
The study, entitled “Secreted frizzled related proteins inhibit fibrosis in vitro but appear redundant in vivo” was published in Fibrogenesis & Tissue Repair by Dr Rik JU Lories’ research group at University Hospitals Leuven in Belgium.
The physiopathology of lung fibrosis is not clear, but it is suggested that the disease is caused by an abnormal repair response, and the disease is associated with significant morbidity and mortality, regardless of the disease’s origin in a patient.
It seems that the activation of signaling pathways that are crucial during embryonic lung development may play a key role in the development of lung fibrosis. There is strong evidence supporting a central role for the activation of wingless-type antagonists like Wnt and transforming growth factor beta (TGFb) signaling pathways in the pathogenesis of lung fibrosis.
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