2004 Degree in Applied Physics, University of Groningen, Netherlands
2005-2008 PhD, University of Padova
2008-2011 Post-Doc Fellow, Venetian Institute of Molecular Medicine
2011-2016 Assistant Professor, Department of Biomedical Sciences, University of Padova
2012-present Group Leader, Veneto Institute of Mol Medicine (VIMM), Padova, Italy
2016-present Associate Professor, Department of Biomedical Sciences, University of Padova, Italy

Personal Statement
Conditions that cause or are complicated by the loss of striated muscle function and mass are a critical health concern and an increasingly prevalent burden on our care system. My main interests are: a) understanding the cellular mechanisms that influence skeletal muscle adaptation in health and disease, and b) developing preventative and therapeutic interventions to reduce the incidence and severity of muscle-related diseases in our communities, placing particular emphasis on the role of exercise. My research places a particular emphasis on new transgenic mouse models impinging on pathways regulating muscle growth and function. In particular, how different intracellular signals regulate muscle contractile properties at different levels, evaluating muscle function in vivo, ex-vivo and in vitro. This approach allows us to identify not only what is regulating muscle mass, but also how muscle function is affected. This aspect is particularly relevant as numerous diseases are characterized by an even more pronounced muscle frailty, than muscle atrophy (i.e. aging, cancer cachexia). This work will hopefully help establish novel interventions to halt or reverse the progression of life-threatening muscle-related disease.

Contributions to Science
Expertise on muscle mass regulation and function, and its link with mTORC1: During this first phase of my independent career I led the work that identified the functional role of mTORC1 in muscle homeostasis and growth. We identified the models, mediators and proteomes under the control of mTORC1 during muscle hypertrophy. In order to better understand the functional role of mTORC1 in adult muscle homeostasis, we generated inducible muscle-specific loss of function mouse models, which we used to show that loss of mTORC1 in skeletal muscle leads to loss of fiber innervation, possibly opening up new avenues to understand why exercise, which activates mTORC1 in muscle, is beneficial for example in aging.
Expertise on muscle activity and exercise: In the lab we set up various approaches to determine muscle function in whole muscles in vivo, isolated muscles ex-vivo, and isolated muscle fibers in vitro. This in-depth analysis of muscle function has allowed us to link changes in muscle signaling or structural proteins to alterations in muscle function, and vice-versa. Using these approaches, we have shown the effect of activity on muscle plasticity in healthy muscle and in different muscular dystrophies