Abstract
Excess fibroblast growth factor (FGF) 23 signaling in patients with chronic kidney disease induces left ventricular hypertrophy. In this issue, Yanucil et al. investigated the interaction of soluble klotho and heparin with FGF23 and FGF receptor isoforms. They concluded that heparin promotes the FGF23–FGF receptor isoform 4 interaction and FGF23 pathogenic effects, supporting an important role of heparin in the pathogenesis of FGF23-mediated left ventricular hypertrophy in chronic kidney disease.
Original language | English (US) |
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Pages (from-to) | 228-230 |
Number of pages | 3 |
Journal | Kidney international |
Volume | 102 |
Issue number | 2 |
DOIs |
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State | Published - Aug 2022 |
Funding
VD received research funding from Akebia Therapeutics and Vifor Pharma and consulting honoraria from Keryx Biopharmaceuticals, Vifor Pharma, Luitpold, and Amgen (outside the submitted work). The other author declared no competing interests. VD was supported by grants from the National Institutes of Health (grant nos. R01DK102815 and R01DK114158).
ASJC Scopus subject areas
- Nephrology