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FGF23 and inflammation-a vicious coalition in CKD
1Division of Nephrology, Department of Medicine, The University of Alabama at Birmingham, Birmingham, Alabama, USA.
Kidney International
|September 24, 2019
Summary
High levels of fibroblast growth factor 23 (FGF23) harm tissues. This study investigates if tumor necrosis factor, an inflammation mediator, increases FGF23 in chronic kidney disease, offering a potential drug target.
Area of Science:
- Endocrinology
- Nephrology
- Inflammation research
Background:
- Elevated fibroblast growth factor 23 (FGF23) serum concentrations are linked to tissue damage.
- In chronic kidney disease (CKD), FGF23 regulation differs from normal physiology.
- Inflammation mediators are explored as contributors to FGF23 elevation in CKD.
Purpose of the Study:
- To investigate the role of tumor necrosis factor (TNF) in elevating FGF23 levels.
- To explore TNF as a potential therapeutic target for reducing FGF23 in CKD.
Main Methods:
- The study focused on analyzing the relationship between TNF and FGF23.
- Specific experimental models or patient cohorts were utilized (details omitted in abstract).
Main Results:
- Preliminary findings suggest a connection between TNF and increased FGF23.
- Further research is needed to confirm TNF's causative role and therapeutic potential.
Conclusions:
- Tumor necrosis factor may contribute to elevated FGF23 in chronic kidney disease.
- Targeting TNF could be a novel strategy for managing FGF23-related complications in CKD.
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