New therapeutic approach to COPD involves targeting and inhibiting protein RIPK1 utsengage
expression increased in alveolar type I , AT2, ciliated and neuroendocrine cells in human COPD. RIPK1 protein levels were significantly increased in airway epithelium of COPD patients, compared to never smokers and smokers without airflow limitation. In mice, exposure to cigarette smoke increasedexpression similarly in AT2 cells, and further in alveolar macrophages and T cells.
. It is published here in its accepted form prior to copyediting and typesetting by our production team. After these production processes are complete and the authors have approved the resulting proofs, the article will move to the latest issue of theConflict of interest: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
Conflict of interest: Tania Maes reports grants from FWO Flanders, Chiesi, GSK; and is a shareholder of Oryzon Genomics, Mendelion Lifesciences SL; outside the submitted work. Conflict of interest: Guy Joos reports consulting fees from GSK, AstraZeneca; lecture honoraria from GSK, AstraZeneca, Novartis, Lapharcon, Eureca vzw; travel support from GSK; and acts as Chair operational Committee IRC for ERS; outside the submitted work.
Conflict of interest: Guy Brusselle reports advisory board participation and lecture honoraria from AstraZeneca, Boehringer-Ingelheim, Chiesi, GlaxoSmithKline, MerchSharp&Dohme, Novartis, Sanofi; outside the submitted work.Received
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