BMP 2016 is designed to expand our understanding of how the BMP signaling axis (BMP/TGFβ/Activin/GDF) influences development and maintenance of organ systems and seeks to uncover how dysregulation of this control results in disease. We challenge attendees to focus on the interconnected nature of the branches of BMP signaling axis, something that is now being considered for the first time and has tremendous implications for understanding diseases of BMP signaling.

BMP 2016 will highlight:

Skeletal biology: BMP superfamily molecules are involved in almost all aspects of bone and cartilage biology. Expanding knowledge of how BMP superfamily signaling impacts the skeletal system creates enormous potential to translate basic research findings into additional successful therapies that improve bone mass or quality, ameliorate diseases of skeletal overgrowth, and repair damage to bones and joints. New discoveries on the role of the BMP signaling axis in the area of skeletal biology will be a central aspect of BMP 2016

Skeletal muscle: Although the importance of myostatin (GDF8) in the regulation of muscle mass is well documented, the finding that inhibition of BMP signaling results in muscle atrophy, abolishes the hypertrophic phenotype of myostatin-deficient mice, and strongly exacerbates the effects of muscle denervation and fasting suggests that under normal physiological circumstances, a balance of inputs by members of the BMP signaling axis is required to maintain muscle mass. New discoveries focused on the interplay between BMP family members in muscle mass regulation and muscle disease will be a central aspect of BMP 2016.

Cardiovascular disease: Perturbation in BMP signaling appear to have a central role in cardiovascular diseases, with evidence of elevated and reduced BMP signaling activity in different disease states. Increased BMP activity is associated with vascular inflammation, atherosclerosis, and calcification as well as anemia of inflammation. Conversely, reduced BMP signaling is associated with pulmonary arterial hypertension (PAH), and hereditary hemorrhagic telangiectasia (HTT). Promising strategies have now been developed to inhibit or enhance BMP signaling in preclinical models of cardiovascular disease and anemia and discussion of these findings will also be a central aspect of BMP 2016.

Neurobiology: BMPs have been shown to have dynamic roles in the nervous system including the ability to regulate early steps of neural patterning, neural stem cell proliferation, and lineage specification. Growing evidence reveals that pathways activated by BMP family signaling molecules play key roles in the establishment of neuromuscular synapses, ensuring proper communication between motor neurons and skeletal muscles, and disturbances in BMP signaling are likely to be associated with a pathogenic status at the muscle fiber or motor neuron. Discussions of the extracellular cues and cellular mechanisms mediated by BMPs in this system will be a central aspect of BMP 2016.

Stem/Progenitor cell biology: An obvious connection between the biological systems listed above is the regulation of stem/progenitor cell populations required to form, maintain, and repair/regenerate each tissue and organ. As members of the BMP signaling axis direct cell fate decisions and are fundamental components of the stem cell niche environment, discussions of the ways in which BMP family members affect stem cell populations will be a central aspect of BMP 2016.

Signaling mechanisms: Central to any investigation of BMP biology is a detailed understanding of the BMP ligand/receptor/co-receptor/antagonist interaction. This topic, like that of stem/progenitor cell biology, provides a connection between the biological systems regulated by BMP axis signaling. Discussion of signaling mechanisms will be a central aspect of BMP 2016.

John, Kuber, Kristi, Paul, Herb and I look forward to seeing you this Fall in Boston!