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

Biographical sketch
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
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:

  1. Dissecting the signaling pathways and cellular processes critical for increasing adult muscle mass and force. Using various new transgenic mouse lines in combination with transcriptomics and proteomics analyses we aim to identify potential new therapeutic targets which can be used to stimulate increase in muscle mass and force.
  2. Determine why muscle function is impaired during cancer-dependent muscle wasting. We have observed that stimulation of specific intracellular signaling pathways can be sufficient to completely revert muscle wasting during cancer cachexia, without affecting tumor size. Furthermore, we have set up a research line evaluating functional properties in muscle fibers taken from patients with different levels of cachexia. Combining these functional analyses with different omics will allow us to identify biomarkers of reduced contractile performance in cancer patients.
  3. Identify the role of skeletal muscle in the systemic beneficial effects of exercise. Here we will address how muscle activity, as occurs during exercise, can affect other organs in the body. Again, using state-of-the-art transgenic mouse models we will determine which muscle-specific factors play a role in the homeostasis of other organs, and how these are modulated by activity.

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
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.
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.

  1. Baraldo M, Nogara L, Dumitras GA, Tchampda Dondjang AH, Geremia A, Scalabrin M, Türk C, Telkamp F, Zentilin F, Giacca M, Krüger M, Blaauw B. Raptor is critical for increasing the mitochondrial proteome and skeletal muscle force during hypertrophy. FASEB Journal, dec 2021
  2. Geremia A, Sartori R, Baraldo M, Nogara L, Balmaceda V, Dumitras GA, Ciciliot S, Scalabrin M, Nolte H, Blaauw B. Activation of Akt-mTORC1 signaling reverts cancer-dependent muscle wasting. Journal of Cachexia, Sarcopenia and Muscle, nov 2021
  3. Blaauw B. Activity-dependent increases of protein synthesis in skeletal muscle: Sensing the energy levels? J Physiol, 2020 May 16
  4. Solagna F, Nogara L, Dyar KA, Greulich F, Mir AA, Türk C, Geremia A, Baraldo M, Sartori R, Farup J, Uhlenhaut H, Vissing K, Kruger M, Blaauw B. Exercise-dependent increases in protein synthesis are accompanied by chromatin modifications and increased MRTF-SRF signalling. Acta Physiologica, 2020 Sep; 230 (1)
  5. Baraldo M, Geremia A, Pirazzini M, Nogara L, Solagna F, Türk C, Nolte H, Romanello V, Megighian A, Boncompagni S, Kruger M, Sandri M, Blaauw B. Skeletal muscle mTORC1 regulates neuromuscular junction stability. Journal of Cachexia, Sarcopenia and Muscle, 2020 Feb;11(1):208-225.
  6. Pozzer D, Varone E, Chernorudskiy A, Schiarea S, Missiroli S, Giorgi C, Pinton P, Canato M, Germinario E, Nogara L, Blaauw B, Zito E. A maladaptive ER stress response triggers dysfunction in highly active muscles of mice with SELENON loss. Redox Biology, Jan 2019; 20:354-366
  7. Pereira MG, Dyar KA, Nogara L, Solagna F, Marabita M, Baraldo M, Chemello F, Germinario E, Romanello V, Nolte H and Blaauw B. Comparative Analysis of Muscle Hypertrophy Models Reveals Divergent Gene Transcription Profiles and Points to Translational Regulation of Muscle Growth through Increased mTOR Signaling. Front Physiol. 2017 Dec 4;8:968. doi: 10.3389/fphys.2017.00968
  8. Blaauw B. Platelet-Derived Growth Factor signaling and the role of cellular crosstalk in functional muscle growth. FEBS Lett. 2017 Mar;591(5):690-692.
  9. Marabita M, Baraldo M, Solagna F, Ceelen JJM, Sartori R, Nolte H, Nemazanyy I, Pyronnet S, Kruger M, Pende M, Blaauw B. S6K1 is required for increasing skeletal muscle force during hypertrophy, Cell Reports, 2016 Oct 4;17(2):501-513.
  10. Dyar KA, Schiaffino S, Blaauw B. Inactivation of the intrinsic muscle clock does not cause sarcopenia. Journal of Physiology Jun 1, 2016; 594(11):3161-2
  11. Dyar KA, Ciciliot S, Malagoli Tagliazucchi G, Pallafacchina G, Tothova J, Argentini C, Agatea L, Abraham R, Ahdesmäki M, Forcato M, Bicciato S, Schiaffino S, Blaauw B. The calcineurin-NFAT pathway controls activity-dependent circadian gene expression in slow skeletal muscle. Molecular Metabolism 2015 Sep 25;4(11):823-33
  12. Blaauw B*, Reggiani C. The role of satellite cells in muscle hypertrophy. J Muscle Res Cell Motil. 2014 Feb 7. [Epub ahead of print]
  13. Blaauw B*, Agatea L, Toniolo L, Canato M, Quarta M, Dyar KA, Danieli-Betto D, Betto R, Schiaffino S, Reggiani C. Eccentric contractions lead to myofibrillar dysfunction in muscular dystrophy. J Appl Physiol. 2010 Jan;108(1):105-11.
  14. Blaauw B*, Canato M, Agatea L, Toniolo L, Mammucari C, Masiero E, Abraham R, Sandri M, Schiaffino S, Reggiani C. Inducible activation of Akt increases skeletal muscle mass and force without satellite cell activation. FASEB J. 2009 Nov;23(11):3896-905.
  1. Research agreement 2019-2022 – Pharmaceutical company
  2. Ricerca Finalizzata, co-P.I. 2019-2022
  3. Research Agreement Sapir 2018-2019– Pharmaceutical company
  4. STARS grant 2018-2020 – University of Padova
  5. AFM research grant 2018-2020 – French Telethòn
  6. MFAG 2018-2023 – Italian Cancer Research Association
  7. BIRD 2017-2019 – Department of biomedical sciences, University of Padova