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2016-to date Associate professor, University of Padua, Italy
2012–to date VIMM group leader
2011–2016 Assistant professor, University of Padua, Italy
2008–2011 Postdoc at the VIMM, Padova, Italy
2005-2008 Ph.D., University of Padua, Italy
1997–2004 Degree in Applied Physics, University of Groningen, Netherlands
I arrived in Italy in 2004 after completing a degree in applied physics at the University of Groningen, the Netherlands. In Padova I performed my PhD in neurobiology and postdoctoral period at the VIMM, before becoming a principal investigator at both the VIMM (2012) and the University of Padova (2011). In 2016 I became associate professor at the University of Padova in the department of Biomedical Sciences.
Electroporation of a constitutively active form of Akt leads to a rapid fiber hypertrophy Field of interest: Adult skeletal muscle is an extremely plastic tissue, rapidly modifying its size and function in response to changes in demands. In the lab we are focusing our attention on the intracellular signaling pathways regulating increases in both mass and function of adult skeletal muscle. Considering the significant problems which arise during aging, disuse and numerous other pathologies leading to muscle atrophy and weakness, together with the well-established beneficial effect of exercise, it is of fundamental importance to understand which pathways regulate muscle growth and how these can be linked to exercise.
Ongoing activities: We have currently three lines of research in the lab:
In all our projects we use a wide range of physiological and molecular biological tools to address these questions in an in-vivo context: electroporation, in vivo and ex vivo muscle force measurements, muscle-specific transgenic and knockout models, ChIP-seq, human muscle biopsies, state-of-the-art microscopy, proteomics, transcriptomics. Many national and international collaborators provide the expertise and technical support for specific parts of the projects.
Future research plans: Mechanisms regulating adult muscle hypertrophy
Basic structure of a skeletal muscle fiber highlights the extreme intracellular organization required to make a well-functioning muscle fiber To prevent skeletal muscle atrophy leading to muscle weakness, as observed in aging, neuromuscular diseases and other pathological conditions, it is essential to get a better understanding of the signaling pathways which regulate skeletal muscle mass and function. Using different newly generated transgenic mouse lines we aim to increase the understanding of the basic changes in protein translation and homeostasis which are critical for muscle growth. These new tools will allow us to better understand the answer to apparently simple questions, yet without an answer currently; 1) Which proteins are important for muscle growth/function after specific stimuli? 2) Where do they localize? 3) When are they made?
Future research plans: How does cancer affect muscle mass and function?
Cancer cachexia is a multi-organ syndrome which is characterized by a strong loss in body weight. It occurs in 50-80% of cancer patients and is due to a drastic loss in muscle and adipose tissue. As cancer cachexia leads to a decrease in physical performance and quality of life, and is associated with poor survival (accounting for more than 20% of cancer deaths), it is of major clinical relevance. Furthermore, cachectic patients show lower response rates to chemotherapy and a reduced tolerance to anticancer treatment. However, despite its clinical importance and the foreseen impact on patients, the pathophysiology of cachexia-associated muscle wasting is still poorly understood preventing the development of specific therapies. In addition, cancer treatments aiming at inhibition of tumor growth are generally given systemically and can therefore also affect the size of other organs, like muscle and adipose tissue.
We are using transgenic mouse models to determine why muscle function is impaired, and how a rescue of only muscle wasting can improve overall well-being and survival of tumor-bearing animals. We are also analyzing muscle biopsies from cancer patients to try and identify markers of muscle dysfunction.
Future research plans: Determine how exercise can affect muscle plasticity and how this leads to systemic improvements
Scheme showing a workflow to analyze muscle function from patients with cancer cachexia. It is well known that exercise has numerous beneficial effects, both by improving muscle performance, but also for numerous other organs. It has become clear the last years that some of the systemic beneficial effects observed after exercise are strictly linked to the changes induced in skeletal muscle. We are currently working on trying to elucidate the signaling changes in skeletal muscle that occur after different types of exercise and how these affect muscle function. On a more systemic level, we have seen that changes in key signaling pathways in skeletal muscle are critical for the maintenance of a healthy nerve-muscle interaction. We are now further expanding this observation and are trying to identify new markers involved in the crosstalk of skeletal muscle with other organs.