Abstract
Searchable abstracts of presentations at key conferences on calcified tissues ISSN 2052-1219 (online)
Highlights
Inhibition of activin/myostatin pathway has emerged as a novel approach to increase muscle mass and bone strength
The role of activins in bone physiology remained unclear until recent studies indicated that inhibition of activin receptor ligands leads to increased bone mass [5, 6]
We aimed to answer the following questions: 1) does inhibition of activin receptor ligands with the use of a soluble activin type IIB-receptor (ActRIIB-Fc) affect bone volume and quality in a muscle dystrophy mouse model [24] parallel to changes in muscle mass and 2) is there an interaction between ActRIIB-Fc treatment and low-intensity aerobic exercise
Summary
Inhibition of activin/myostatin pathway has emerged as a novel approach to increase muscle mass and bone strength. The role of activins in bone physiology remained unclear until recent studies indicated that inhibition of activin receptor ligands leads to increased bone mass [5, 6]. In these experiments, soluble activin receptor-Fc fusion proteins were used as decoy receptors harvesting and inhibiting their ligands including activin A and myostatin. Soluble activin receptor-Fc fusion proteins were used as decoy receptors harvesting and inhibiting their ligands including activin A and myostatin These studies suggested that inhibition of activin pathway could be a promising therapeutic target for metabolic bone diseases [7]. Increasing body weight through muscle mass in combination with exercise has not been investigated before
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