A new protein curbs the hypertrophic effect of myostatin inhibition, adding remarkable endurance to motor performance in mice

• DOI: 10.1371/journal.pone.0228653
• Publication Date: 2020-03-11T13:39:15Z
• Authors: Marina Boido; Olena Butenko; Consuelo Filippo; Roberta Schellino; Jan W. Vrijbloed; Ruggero G. Fariello; Alessandro Vercelli
• Keywords: Myostatin; Agrin; Activin receptor

Current efforts to improve muscle performance are focused on trophism via inhibition of the myostatin pathway: however they have been unsuccessful in clinic date. In this study, a novel protein has created by combining soluble activin receptor, strong inhibitor, C-terminal agrin nLG3 domain (ActR-Fc-nLG3) involved development and maintenance neuromuscular junctions. Both domains connected constant region an Igg1 monoclonal antibody. Surprisingly, young male mice treated with ActR-Fc-nLG3 showed remarkably increased endurance rotarod test, significantly longer than single compounds ActR-Fc Fc-nLG3 animals. This increase was accompanied only moderate body weights wet animals were lower expected. The inhibitor induced, as expected, highly significant compared control Moreover, prolonged effect not observed when dosed simultaneously mixture these very similar animals, indicating that both need be one molecule. Muscle morphology induced did appear changed however, close examination junction acetylcholine receptor surface area for controls. result is consistent published observations training rats quantity at junctions provide evidence improving nerve-muscle interaction could important factor sustaining long term activity.