Is FGF23 or FGF21 a Promising Biomarker to Indicate the Aging Process in COPD?

Recently, we read with great interest the paper entitled "Various Mechanistic Pathways Representing the Aging Process Are Altered in COPD" in CHEST (January 2016) by Rutten et al,1 in which the authors showed in an excellent work that several biomedical signaling pathways were probably involved in the aging process of patients with COPD. Interestingly, soluble klotho significantly decreased in patients with COPD compared with those in the smoking or nonsmoking control groups. It has been widely recognized that klotho has two subunits consisting of α-klotho and β-klotho that separately trigger distinct physiological actions by binding to its coreceptors fibroblast growth factor (FGF) 23 and FGF21.2 Although FGF23 and FGF21 are individually implicated in the pathogenesis of chronic kidney disease and obesity,3 it cannot be ignored that abnormalities in FGF23 or FGF21, or both, would also be implicated in the underlying mechanisms of the aging process in COPD. More importantly, klotho deficiency may elicit a vicious result of resistance of FGF 23 and FGF21, since decreased klotho could not provide adequate binding sites for FGF 23 and FGF21.2,3 Relative increased levels of FGF23 and FGF21 would exert deletion effects on physiological functions.3 Based on these findings, we suggest that excessive levels of FGF23 or FGF21, or both, are also probably involved in the mechanisms of the COPD-related aging process. It is likely, therefore, that detecting levels of FGF23 or FGF21, or both, may favor the observation of the aging process of individuals with COPD. To the best of our knowledge, there is no study reporting the role of FGF23 or FGF21 in COPD. Subsequent investigations on the role of FGF-klotho signaling in the COPD-associated aging process are needed.

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