LAUSR

lung injury and fibrosis. Exposure to g -radiation, an experimental model of pulmonary fibrosis, can cause tissue injury associated with release of DAMPs. eNAMPT is a novel DAMP that can aggravate proinflammatory responses. Garcia and colleagues show that eNAMPT release contributes to radiation-induced pulmonary fibrosis (RIPF) in mice. The release of eNAMPT can activate inflammatory cells within the profibrotic niche via activation of TLR4. eNAMPT may also potentially activate fibroblasts/myofibroblasts indirectly via macrophage-dependent inflammation or also directly via TLR4 activation. Direct or indirect activation via cross-talk of other pulmonary cell types by eNAMPT, such as AT1 or AT2, warrants further investigation. Collectively activation of inflammatory cells, fibroblasts/myofibroblasts and other cell types within the alveolar niche may promote profibrotic responses. The studies of Garcia and colleagues further show that blocking eNAMPT can reduce tissue injury and fibrosis in models of RIPF, implicating eNAMPT as an attractive therapeutic target in IPF and other fibrotic lung diseases. AT1, AT2=Type I or Type II epithelial cells; eNAMPT=extracellular nicotinamide phosphoribosyltransferase; mAb=monoclonal antibodies; RIPF=radiation-induced pulmonary fibrosis; TRL4=Toll-like receptor-4.