MYOS RENS is evaluating the genotypic characteristics and molecular pathways that contribute to the changes seen in muscle and inflammatory disease states associated with sarcopenia and related disorders. We are investigating the role of many signaling pathways including activin A, myostatin and follistatin on fundamental biologic processes important in the repair and regeneration of muscle tissue, including those regulating proliferation and differentiation of primary myoblasts. Our research also examines the role of natural and synthetic molecules, including follistatin in regulating myostatin activity, as well as how myostatin modulation effects the growth, retention and repair of lean muscle.
In particular, we are using a systems biologic and metabolic analytic approach to establish the genetic and molecular basis for understanding the regulation of muscle growth and repair. We are using these methods to determine the role of myostatin and other regulatory molecules in the complex communication between skeletal muscle and adipose tissue and their involvement in age-related sarcopenia, disease associated cachexia, diabetes and other complex systemic metabolic diseases including anorexia nervosa. Our collaborative efforts with scientist and physicians from world-class universities and institutions include Harvard Medical School, Hackensack University Medical Center, and GNS Healthcare.
Scientific efforts focus on understanding the mechanisms of action that lead to disease states affecting muscle and inflammation. The foundation of our basic science research program evaluates the targets and process that lead to muscle and inflammatory disease states.
Our product development is based on the understanding that myostatin antagonists and inhibitors are likely to enhance both muscle mass and bone strength. Myostatin is capable of inducing muscle atrophy via its inhibition of myoblast proliferation, increasing ubiquitin proteasomal activity and down-regulating activity of the IGF-Akt pathway.
These well-recognized effects are seen in multiple atrophy causing situations, including injury, diseases such as cachexia, disuse and space flight, demonstrating the importance of the myostatin signaling mechanism.
Myostatin also plays a role in disrupting the metabolic homeostasis that promotes healthy cell growth and regulates inflammation linked to diabetes, obesity, certain forms of heart disease and cancers.