Krick S, et al. - Researchers investigated if fibroblast growth factor (FGF) 23 and klotho-mediated FGFR activation delineates a pathophysiologic mechanism in chronic obstructive pulmonary disease (COPD), presuming that FGF23 can potentiate airway inflammation via klotho independent FGFR4 activation. They used plasma and transbronchial biopsies from COPD and control patients and primary human bronchial epithelial cells from COPD patients as well as a murine COPD model in order to study FGF23 and its impact. They found that in COPD, airway inflammation was induced by cigarette smoke by downregulation of klotho and activation of FGFR4 in the airway epithelium. In COPD, inhibition of FGF23 or FGFR4 might serve as a novel anti-inflammatory strategy.