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Klotho is upregulated in human cardiomyopathy independently of circulating Klotho levels

G Poelzl1, S K Ghadge1, M Messner1

  • 1Department of Internal Medicine III, Cardiology and Angiology, Medical University of Innsbruck, Innsbruck, Austria.

Scientific Reports
|June 1, 2018
PubMed

Insights

Fibroblast growth factor 23 (FGF23) levels predict chronic heart failure progression. Soluble Klotho (sKlotho) in serum does not, but Klotho is upregulated in diseased hearts, suggesting local effects.

Area of Science:

  • Cardiology
  • Endocrinology
  • Gerontology

Background:

  • Klotho is an antiaging protein with known cardioprotective effects.
  • Trans-membrane Klotho functions as a fibroblast growth factor 23 (FGF23) co-receptor in the kidney.
  • Soluble Klotho (sKlotho) offers cardioprotection against systolic dysfunction, independent of FGF23.

Purpose of the Study:

  • To investigate the association between FGF23, sKlotho, and chronic heart failure (CHF) progression.
  • To analyze Klotho expression in human heart tissue from patients with cardiomyopathy (CMP).

Main Methods:

  • Serum levels of sKlotho and FGF23 were measured in 287 CMP patients.
  • Klotho mRNA and protein expression were analyzed in human CMP and control heart tissues.
  • Immunoblotting was used to confirm sKlotho upregulation and protease expression.

Main Results:

  • Patients in the lowest FGF23 tertile had a 4.1-fold higher likelihood of remaining free from adverse outcomes.
  • No correlation was found between serum sKlotho levels and the combined endpoint.
  • Klotho mRNA was upregulated in human CMP hearts, with increased sKlotho and associated proteases.

Conclusions:

  • Serum FGF23, but not sKlotho, is associated with chronic heart failure progression.
  • Klotho is upregulated in diseased hearts, indicating potential local paracrine functions.
  • These findings suggest distinct roles for FGF23 and local Klotho in heart failure pathophysiology.

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