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The Complexity of FGF23 Effects on Cardiomyocytes in Normal and Uremic Milieu

Andreja Figurek1,2, Merita Rroji3, Goce Spasovski4

  • 1Department of Internal Medicine, Medical Faculty, University of Banja Luka, 78000 Banja Luka, Republic of Srpska, Bosnia and Herzegovina.

Cells
|June 2, 2021
PubMed

Insights

Fibroblast growth factor-23 (FGF23) is a key predictor of cardiovascular risk, especially in chronic kidney disease (CKD). This review explores FGF23

Area of Science:

  • Cardiovascular Research
  • Nephrology
  • Endocrinology

Background:

  • Fibroblast growth factor-23 (FGF23) is increasingly recognized as a significant biomarker.
  • Elevated FGF23 levels are linked to cardiovascular complications, particularly in patients with chronic kidney disease (CKD).
  • Understanding FGF23's role in cardiac function is crucial for managing cardiovascular risk.

Purpose of the Study:

  • To review the mechanisms of FGF23 action in the myocardium.
  • To examine FGF23's role in both physiological and pathophysiological states of CKD.
  • To discuss FGF23's interactions with other signaling pathways in cardiomyocytes.

Main Methods:

  • Literature review of existing studies on FGF23.
  • Analysis of FGF23's effects on myocardial tissue.
  • Examination of FGF23's signaling pathways and cross-talk.

Main Results:

  • FGF23 influences myocardial function through various signaling pathways.
  • CKD exacerbates the detrimental effects of FGF23 on the heart.
  • FGF23 interacts with other critical signaling cascades within cardiomyocytes.

Conclusions:

  • FGF23 is a critical mediator of cardiovascular risk in CKD.
  • Targeting FGF23 pathways may offer novel therapeutic strategies.
  • Further research into FGF23's cardiac mechanisms is warranted.

Keywords:
FGF signalingFGF23Wnt pathwaycardiomyocyteklotho

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