Myostatin inhibition and upregulation of the myostatin inhibitor follistatin are approaches to spurring increased muscle growth. This class of approach has been shown to work in humans to at least some degree, and there are numerous heavily muscled myostatin loss of function mutants in various animal species, both naturally occurring and created via genetic technologies. SMAD2 is a related regulatory protein, and some efforts to increase muscle growth have targeted it. Further exploration in this same cluster of regulatory proteins leads to JNK, the subject of today’s open access paper.
This portion of mammalian biochemistry is an area of interest to researchers as a potential means to treat sarcopenia, the characteristic loss of muscle mass and strength that occurs with aging. If muscle growth can be dialed up as needed, something that seems a plausible goal at this point, then that capability would deal with half of the problem of sarcopenia, leaving just the quality of the muscle to be addressed. It might also be deployed as a compensatory therapy for forms of muscle wasting, such as that occurring as a result of cancer and its treatment. Of course, one suspects that use