One of the first studies that confirmed my BMP hypothesis. The timing was beautiful, as it came a few months after the initial design was complete. This was an exhilarating time, as there wasn't a whole lot for me to work off of.
Why am I posting this? Well, this is a very simple understanding. As well, to draw attention to the BMP-Myostatin connection for the upcoming, VERY EXCITING, MyoSynergy announcement.
Those lucky enough to have experienced the original BMP/MyoSynergy stack are in for a treat.
Invalid Link Removed 2013 Nov;45(11):1309-18. doi: 10.1038/ng.2772. Epub 2013 Sep 29.
BMP signaling controls muscle mass.
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Abstract
Cell size is determined by the balance between protein synthesis and degradation. This equilibrium is affected by hormones, nutrients, energy levels, mechanical stress and cytokines. Mutations that inactivate myostatin lead to excessive muscle growth in animals and humans, but the signals and pathways responsible for this hypertrophy remain largely unknown. Here we show that bone morphogenetic protein (BMP) signaling, acting through Smad1, Smad5 and Smad8 (Smad1/5/8), is the fundamental hypertrophic signal in mice. Inhibition of BMP signaling causes muscle atrophy, abolishes the hypertrophic phenotype of myostatin-deficient mice and strongly exacerbates the effects of denervation and fasting. BMP-Smad1/5/8 signaling negatively regulates a gene (Fbxo30) that encodes a ubiquitin ligase required for muscle loss, which we named muscle ubiquitin ligase of the SCF complex in atrophy-1 (MUSA1). Collectively, these data identify a critical role for the BMP pathway in adult muscle maintenance, growth and atrophy.
PMID: 24076600 DOI: Invalid Link Removed
[Indexed for MEDLINE]