Serge Ferrari (MD) graduated from Geneva Medical School in 1989 and was a Research and Clinical Fellow and Lecturer in Medicine at Harvard Medical School from 1997-2001. He has received a professorship grant from the Swiss National Science Foundation and is currently Full Professor of Medicine and Vice Dean for Translational Research and Innovation at the Geneva Faculty of Medicine. He is Director of the Service and Research Laboratory of Bone Diseases at the University Hospital of Geneva. He is immediate past president of the Swiss Society for Osteoporosis and a member of the Scientific Committee of the Novartis Foundation for Medicine-Biology. He has been continuously funded by the SNF for more than 25 years, has published more than 300 articles and book chapters in the field of osteoporosis, bone and mineral metabolism, and was recently awarded the prestigious Lawrence J. Raisz Award for Translational Research by the American Society of Bone and Mineral Research.

Research aims

Mechanisms of bone fragility in diabetes

Professor Ferrari's group uses biochemistry, cell culture, mouse genetics and human cohorts to study the pathophysiology of diabetes-induced bone fragility. Osteocytes, the long-lived cells that reside within the bone matrix, orchestrate bone modelling and remodelling in response to mechanical loading and hormones. Recent evidence suggests that osteocyte functions are defective in type 1 (T1D) and type 2 diabetes (T2D). Therefore, we are now investigating the role of insulin signalling in osteocytes in the context of T1D (Akita mice) and T2D (HFD + streptozotocin mice). In addition, they investigate how reduced autophagy, altered mitochondria-associated endoplasmic reticulum membranes and excessive PDGFRβ signalling in osteocytes contribute to the pathogenesis of T2D-induced bone fragility (HFD + STZ). Finally, they use proteomic analyses of sera from a cohort of patients with metabolic syndrome and T2D to identify novel markers of T2D-induced bone fragility.