Dysregulated Klotho and FGF23 signaling aggravates vascular remodeling in age-related pulmonary hypertension.

Paul-Lennard Perret, Jonathan H Kim, Annika Winkler, Christiane Ott, Willem Bintig, Teresa C Funk-Hilsdorf, Erik Asmus, Szandor Simmons, Laura Michalick, Philip D Solymosi, Petra Knaus, Catrin Herpich, Kristina Norman, Ursula Müller-Werdan, Vasile Foris, Gabor Kovacs, Makoto Kuro-O, Tilman Grune, Jakob Voelkl, Jana Grune, Wolfgang M Kuebler

Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Charitéplatz 1, 10117 Berlin, Germany.Charité-Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Charitéplatz 1, 10117 Berlin, Germany. · pubmed

Paper

Abstract

Pulmonary arterial hypertension (PAH) is a chronic condition of elevated pulmonary arterial pressure caused by vascular remodeling 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 model and analyses of human cohorts, we probed for a role of the anti-aging protein Klotho which acts as co-receptor for fibroblast growth factor 23 (FGF23) in the pathogenesis of PAH.

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Research summary

The paper claims that dysregulated Klotho and FGF23 signaling contributes to vascular remodeling in age-related pulmonary hypertension. The research addresses mechanisms related to aging and the role of specific proteins in age-related diseases, which aligns with longevity research.

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