Matthew Blake Greenblatt   Associate Professor of Pathology and Laboratory Medicine

  • +1 212 746 2040


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  • Approximately half of all women and a fifth of all men will experience a skeletal fracture due to low bone mass.  These fractures kill as many women each year as breast cancer. Improving clinical outcomes in this area will ultimately require finding new therapeutic agents that promote the activity of osteoblasts, the cells that build bone, which in turn will require improving our understanding of the molecular pathways involved in this process.  To this end, we are focused on using a combination of genetics, cellular biochemistry and genome-wide screening to discover new molecular pathways that regulate the activity of osteoblasts.  In particular, we have focused on how osteoblasts shape their supporting tissues in bone, such as skeletal vascular endothelium, to identify SLIT3 as an osteoblast derived angiogenic factor.  Through the ability to induce pro-osteogenic forms of skeletal vascular endothelium SLIT3 functions as a novel osteoanabolic agent.     Our other major area of interest is identifying the cell types that comprise bone through a combination of flow cytometry, single cell sequencing and transplantation-based functional studies. 

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  • Matthew Blake Greenblatt

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