Osteologie 2021; 30(04): 339
DOI: 10.1055/s-0041-1736723
Abstract

Inhibition of Foxo3 during myogenic differentiation

E Rodenwaldt
1   Klinik für Unfallchirurgie, Orthopädie und Plastische Chirurgie der Universitätsmedizin Göttingen, Göttingen
,
B Gellhaus
1   Klinik für Unfallchirurgie, Orthopädie und Plastische Chirurgie der Universitätsmedizin Göttingen, Göttingen
,
M Gsaenger
1   Klinik für Unfallchirurgie, Orthopädie und Plastische Chirurgie der Universitätsmedizin Göttingen, Göttingen
,
R Kosinsky
2   Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, MN, USA
,
O K Böker
1   Klinik für Unfallchirurgie, Orthopädie und Plastische Chirurgie der Universitätsmedizin Göttingen, Göttingen
,
F A Schilling
1   Klinik für Unfallchirurgie, Orthopädie und Plastische Chirurgie der Universitätsmedizin Göttingen, Göttingen
,
D Saul
1   Klinik für Unfallchirurgie, Orthopädie und Plastische Chirurgie der Universitätsmedizin Göttingen, Göttingen
3   Mayo Clinic, Division of Endocrinology, Diabetes and Nutrition, Rochester, MN, USA
› Author Affiliations
 

Introduction

Patients suffering from disease-related (secondary) sarcopenia have been associated with an enhanced level of the transcription factor Foxo3 in skeletal muscle [1] [2] [3].

Sarcopenia is a progressive and generalized muscle disorder characterized by a decline in muscle mass and strength [4]. If left untreated, it can lead to increased falls, fractures [5] [6], mortality [7], reduced quality of life [8], as well as increased hospitalization rates and cost of care [9].

Foxo3 is one of several transcription factors of the highly conserved Forkhead-Box-Protein family [10]. As a downstream target of the PI3K/AKT pathway [11], Foxo3 plays an important role in protein turnover and muscle wasting [12]. Foxo3 therefore could pose to be a potential target of treatment for secondary sarcopenia.

The focus of this study is to reduce the Foxo3-expression in murine myoblasts in vitro and to analyze changes in myogenic differentiation.



Publication History

Article published online:
04 November 2021

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