Science and Research

Dysregulated Klotho and FGF23 signalling aggravates vascular remodelling in age-related pulmonary hypertension

AIMS: Pulmonary arterial hypertension (PAH) is a chronic condition of elevated pulmonary arterial pressure caused by vascular remodelling due to increased proliferation of pulmonary arterial smooth muscle cells (PASMC). Initially described as a disease primarily affecting young women, it now increasingly affects the elderly. Age-related pathomechanisms of PAH remain, however, unclear. In a translational approach combining preclinical disease models and analyses of human cohorts, we probed for a role of the anti-ageing protein Klotho, which acts as a co-receptor for fibroblast growth factor 23 (FGF23) in the pathogenesis of PAH. METHODS AND RESULTS: Mice aged 114-117 weeks showed moderate spontaneous PAH with right ventricular (RV) hypertrophy and dysfunction relative to young mice aged < 40 weeks. This effect was further pronounced upon hypoxic exposure (10% O2) for 14 days. Histological sections showed pulmonary vascular wall thickening of small pulmonary arterioles. Similar findings were obtained in mice with a partial Klotho deficiency (kl/+) that developed RV systolic pressures (RVSP) of 72.58 +/- 3.3 mmHg within two weeks of hypoxia. Aged mice and kl/+ mice had elevated plasma levels of FGF23, further amplified by hypoxic exposure. ELISA-based measurements in serum of patients from a cross-sectional study with PAH aged 60 years or older confirmed an increase in circulatory FGF23. Immunohistochemistry staining of lung tissue showed increased proliferative activity of PASMC in kl/+ mice, and recombinant FGF23 elevated proliferative activity of PASMC in vitro. The hyperproliferative response to FGF23 was prevented by siRNA-mediated knockdown of fibroblast growth factor receptor 1 in PASMC. In kl/+ mice, FGF23 neutralisation using an anti-FGF23 antibody reduced RVSP, improved RV dysfunction and RV hypertrophy and prevented pulmonary vascular remodelling. CONCLUSION: Our findings identify the accumulation of FGF23 as novel mechanism of pulmonary vascular remodeling in PAH. Targeting dysregulated Klotho/FGF23 signalling may present a promising therapeutic strategy in elderly patients.

  • Perret, P. L.
  • Kim, J. H.
  • Winkler, A.
  • Ott, C.
  • Bintig, W.
  • Funk-Hilsdorf, T. C.
  • Asmus, E.
  • Simmons, S.
  • Michalick, L.
  • Solymosi, P. D.
  • Knaus, P.
  • Herpich, C.
  • Norman, K.
  • Muller-Werdan, U.
  • Foris, V.
  • Kovacs, G.
  • Kuro, O. M.
  • Grune, T.
  • Voelkl, J.
  • Grune, J.
  • Kuebler, W. M.

Keywords

  • Animals
  • Klotho Proteins
  • Fibroblast Growth Factor-23
  • *Vascular Remodeling
  • *Fibroblast Growth Factors/metabolism/genetics/blood
  • Signal Transduction
  • Humans
  • Disease Models, Animal
  • *Pulmonary Artery/physiopathology/metabolism/pathology
  • *Glucuronidase/genetics/metabolism/deficiency
  • *Pulmonary Arterial Hypertension/physiopathology/metabolism/pathology/genetics
  • Male
  • Mice, Inbred C57BL
  • Ventricular Function, Right
  • Age Factors
  • *Hypertrophy, Right Ventricular/physiopathology/metabolism/genetics/pathology
  • Female
  • Myocytes, Smooth Muscle/metabolism/pathology
  • *Ventricular Dysfunction, Right/physiopathology/metabolism/genetics/pathology
  • Mice, Knockout
  • Middle Aged
  • *Muscle, Smooth, Vascular/metabolism/pathology/physiopathology
  • *Arterial Pressure
  • Aged
  • Cell Proliferation
  • Cells, Cultured
  • Hypoxia/complications/physiopathology
  • *Hypertension, Pulmonary/physiopathology/metabolism/pathology
  • Ageing
  • Fgf23
  • Klotho
  • Pulmonary arterial hypertension
  • Smooth muscle cells
  • Vascular remodelling
Publication details
DOI: 10.1093/cvr/cvag048
Journal: Cardiovasc Res
Pages: 764-777 
Number: 6
Work Type: Original
Location: Assoziierter Partner
Disease Area: PH
Partner / Member: BIH
Access-Number: 41749458
See publication on PubMed


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