Fibroblast Growth Factor-23 and Hypophosphatemia in Chronic Obstructive Pulmonary Disease Patients

Elsammak, Mohamed; Attia, Adel; Suleman, Moosa

doi:10.2478/v10011-011-0031-5

Cited by 14 publications

(15 citation statements)

References 23 publications

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“…However, in this study the smokers were not further characterized regarding COPD. In a different report, increased FGF23 levels in COPD patients were linked to hypophosphatemia, but a mechanism for elevation and the source of circulating FGF23 was not identified (30). Here, we show that FGF23 levels appear not to correlate with disease severity per se, since there is no systemic FGF23 elevation in patients with severe COPD.…”

Section: Discussionmentioning

confidence: 99%

Fibroblast growth factor 23 and Klotho contribute to airway inflammation

et al. 2018

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Circulating levels of fibroblast growth factor (FGF) 23 are associated with systemic inflammation and increased mortality in chronic kidney disease. α-klotho, a co-receptor for FGF23, is downregulated in chronic obstructive pulmonary disease (COPD). However, whether FGF23 and klotho-mediated FGFR activation delineates a pathophysiologic mechanism in COPD remains unclear. We hypothesized that FGF23 can potentiate airway inflammation via klotho independent FGFR4 activation. FGF23 and its effect were studied using plasma and transbronchial biopsies from COPD and control patients and primary human bronchial epithelial cells isolated from COPD patients as well as a murine COPD model. Plasma FGF23 levels were significantly elevated in COPD patients. Exposure of airway epithelial cells to cigarette smoke and FGF23 led to a significant increase in IL-1β release via klotho-independent FGFR4-mediated activation of phospholipase Cγ (PLCγ)/nuclear factor of activated T-cells (NFAT) signaling. In addition, klotho knockout mice developed COPD and showed airway inflammation and elevated FGFR4 expression in their lungs, whereas overexpression of klotho led to an attenuation of airway inflammation. In conclusion, cigarette smoke induces airway inflammation 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 in COPD.

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Section: Discussionmentioning

confidence: 99%

Fibroblast growth factor 23 and Klotho contribute to airway inflammation

et al. 2018

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“…The surfactant-associated protein gene has been used as candidate gene in studies on the genetics of RDS. The polymorphism and mutation of SP-B have been found to be related to the RDS (15,16). SP-B is a hydrophobic protein synthesized in type II alveolar cells.…”

Section: Discussionmentioning

confidence: 99%

Expression of Pulmonary Surfactant-Associated Protein B in Neonatal Respiratory Distress Syndrome

Yin¹,

Wang²,

Xie³

et al. 2013

Journal of Medical Biochemistry

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SummaryBackground: The aim of this study was to investigate the role of pulmonary surfactant-associated protein B (SP-B) expression in the pathogenesis of neonatal respiratory distress syndrome (RDS) via detecting the protein and mRNA expression of SP-B. Methods: A total of 60 unrelated neonates who died of RDS were chosen as the RDS group and then subgrouped into ≤32 weeks group, 32∼37 weeks group and ≥37 weeks group (n=20). Sixty neonates who died of other diseases were enrolled as controls and subdivided into 3 matched groups based on the gestational age. Western blot assay and RT-PCR were employed. Results: In the RDS group, SP-B protein expression was reduced or deficient in 8 neonates of which 6 had no SP-B protein expression. In the control group, only 1 had reduced SP-B protein expression. The reduced or deficient SP-B protein expression in 9 neonates of both groups was noted in the ≥37 weeks group. In the RDS group, the SP-B mRNA expression was significantly lower than that in the control group. In the ≤37 weeks group, SP-B mRNA expression was comparable between the RDS group and control group. In the 32∼37 weeks group, the SP-B mRNA expression in the RDS group was significantly reduced when compared with the control group. In the ≥37 weeks group, the SP-B mRNA expression in the RDS group was dramatically lower than that in the control group. Conclusions: Alteration of SP-B expression is present at transcriptional and translational levels. Reduction of SP-B mRNA and protein expression is involved in the pathogenesis of RDS.

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“…Further renal conditions including fibrosis , albuminuria and autosomal dominant polycystic kidney disease (ADPKD) are associated with elevated FGF23 levels. Also, impaired liver function and lung disease stimulate FGF23 production. Patients with heart failure or atherosclerosis have higher FGF23 levels.…”

Section: Fgf23 Regulation: Insights From Rare Disorders and Renal Dismentioning

confidence: 99%

Regulation of fibroblast growth factor 23 (FGF23) in health and disease

et al. 2019

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Fibroblast growth factor 23 (FGF23) is mainly produced in the bone and, upon secretion, forms a complex with a FGF receptor and coreceptor αKlotho. FGF23 can exert several endocrine functions, such as inhibiting renal phosphate reabsorption and 1,25‐dihydroxyvitamin D3 production. Moreover, it has paracrine activities on several cell types, including neutrophils and hepatocytes. Klotho and Fgf23 deficiencies result in pathologies otherwise encountered in age‐associated diseases, mainly as a result of hyperphosphataemia‐dependent calcification. FGF23 levels are also perturbed in the plasma of patients with several disorders, including kidney or cardiovascular diseases. Here, we review mechanisms controlling FGF23 production and discuss how FGF23 regulation is perturbed in disease.

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Fibroblast Growth Factor-23 and Hypophosphatemia in Chronic Obstructive Pulmonary Disease Patients

Cited by 14 publications

References 23 publications

Fibroblast growth factor 23 and Klotho contribute to airway inflammation

Fibroblast growth factor 23 and Klotho contribute to airway inflammation

Expression of Pulmonary Surfactant-Associated Protein B in Neonatal Respiratory Distress Syndrome

Regulation of fibroblast growth factor 23 (FGF23) in health and disease

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