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Updated: Feb 24, 2026

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Decreased Expression of Thrombomodulin in Endothelial Cells by Fibroblast Growth Factor-23/α-Klotho

Kenji Tanaka1, Tancharoen Salunya2, Yoshihiro Motomiya1

  • 1Suiyukai Clinic, Kashihara, Nara, Japan.

Therapeutic Apheresis and Dialysis : Official Peer-Reviewed Journal of the International Society for Apheresis, the Japanese Society for Apheresis, the Japanese Society for Dialysis Therapy
|August 24, 2017
PubMed

Insights

Excessive fibroblast growth factor-23 (FGF23) in chronic kidney disease (CKD) may damage blood vessels by reducing thrombomodulin (TM). This finding offers a new explanation for cardiovascular risks in hemodialysis patients.

Area of Science:

  • Nephrology
  • Cardiovascular Research
  • Endothelial Biology

Background:

  • Chronic kidney disease (CKD) is linked to high fibroblast growth factor-23 (FGF23) and low α-Klotho.
  • Hemodialysis patients face increased cardiovascular disease and endothelial dysfunction mortality.
  • The FGF23-endothelial damage link in CKD remains unclear.

Purpose of the Study:

  • Investigate the effect of FGF23 on thrombomodulin (TM) in endothelial cells.
  • Explore the role of FGF23/α-Klotho in endothelial barrier integrity.
  • Elucidate a potential mechanism for cardiovascular risk in CKD patients.

Main Methods:

  • Stimulated human umbilical vein endothelial cells with FGF23 and FGF23/α-Klotho.
  • Measured membrane-bound TM levels.
  • Quantified soluble TM in cell supernatants.

Main Results:

  • FGF23 and FGF23/α-Klotho suppressed membrane TM in a dose-dependent manner.
  • Soluble TM levels, indicating endothelial injury, were elevated post-stimulation.
  • Demonstrated a direct impact of FGF23 on endothelial TM.

Conclusions:

  • Excessive FGF23 may disrupt endothelial TM, contributing to cardiovascular risk in CKD.
  • This mechanism highlights FGF23's role in endothelial dysfunction in hemodialysis patients.
  • Findings provide insights into CKD-associated cardiovascular complications.

Keywords:
Fibroblast growth factor-23HUVECHemodialysis patientsThrombomodulinα-Klotho

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