作者: Nicola J Lomas , Monica A Spiteri , Nicholas R Forsyth , Khondoker M Akram
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摘要: Idiopathic pulmonary fibrosis (IPF) is a progressive, debilitating, and fatal lung disease of unknown aetiology with no current cure. The pathogenesis IPF remains unclear but repeated alveolar epithelial cell (AEC) injuries subsequent apoptosis are believed to be among the initiating/ongoing triggers. However, precise mechanism apoptotic induction hitherto elusive. In this study, we investigated expression panel pro-apoptotic cycle regulatory proteins in 21 19 control tissue samples. We reveal significant upregulation apoptosis-inducing ligand TRAIL its cognate receptors DR4 DR5 AEC within active lesions lungs. This was accompanied by protein p53 overexpression. contrast, myofibroblasts fibroblastic foci lungs exhibited high TRAIL, negligible expression. Similarly, absent or macrophages lymphocytes. No differences were noted these types between detected marker cellular senescence p21WAF1 upregulated affected Cell Cyclin D1 SOCS3 significantly enhanced remodelled fibrotic areas myofibroblasts. Taken together findings suggest that, IPF, can display markers associated proliferation, senescence, apoptotosis, where could drive response. Clear understanding processes identification therapeutic targets will direct us develop effective therapies for IPF.