Cristina Mammucari
Cristina Mammucari
affiliation: Università di Padova
research area(s): Cell Biology
Course: Biosciences and Biotechnologies
University/Istitution: Università di Padova
Assistant Professor of General Pathology, Department of Biomedical Science, University of Padova.

February 2004
PhD in Cell and Molecular Biology (Università di Torino, Italy).
May 1999
License of Pharmacist.
October 1998
Master degree in Pharmaceutical Chemistry and Technology, cum laude (Università degli Studi di Padova, Italy).

January 2009-present
Role of mitochondrial calcium signalling in physiopathology: influence on skeletal muscle homeostasis and triple negative breast cancer metastasis.
March 2005-December 2008
Post-doctoral fellow.
Venetian Institute of Molecular Medicine (VIMM), Padova, Italy. Supervisor: S. Schiaffino.
Research topic: role of Akt-FoxO pathway in the regulation of muscle autophagy and as a therapeutic strategy for muscular dystrophies.
January 2003- February 2005
Graduate student (until February 2004) and post-doctoral fellow.
Institut de Biochimie, Université de Lausanne, Switzerland. Supervisor: Gian Paolo Dotto.
Research topic: mouse keratinocytes growth and differentiation control: integration of Notch1 and Calcineurin/NFAT signaling pathways.
September 1999-December 2002
Graduate student.
Cutaneous Biology Research Center, Massachusetts General Hospital and Harvard Medical School, Charlestown, USA. Supervisor: Gian Paolo Dotto.
Research topic: mouse keratinocytes growth and differentiation control: identification of a novel Notch-interacting protein and its role in the modulation of Notch-1 function.
November 1997-September 1999
Undergraduate student (nov 1997-oct 1998) and research assistant (nov 1998-sept 1999)
Department of Pharmaceutical Sciences, Università degli Studi di Padova, Italy.
Reseach topic: Drug and enzyme controlled release from polymeric hydrogels.
September 1996-December 1996
Undergraduate student (”Erasmus” fellowship).
Department of Chemistry of North Wales, Bangor, UK.
Synthesis of acetals between pyruvate derivatives and 1,3-butanediol (and derivatives).

January 2009-present
Genetic Pathology and Physiopathology for Biotechnology undergraduate students;
General Pathology for Obstetrics undergraduate students;
General Pathology for Clinical Pathology and Food Science graduate students;
Histopathology lab assistant for medical students.
PhD program in biology and biotechnology.
January 2003-February 2005
Biochemistry laboratory for medical students at the University of Lausanne.

Award for poster presentation: Gordon Research Conference “Autophagy in stress, development and disease”, Ventura, CA, (USA), January 2008.
Award for poster presentation: “4th International Symposium on Autophagy”, Mishima, Japan, October 2006.
CRS Award in recognition of outstanding poster presentation, "Drug Delivery for the Third Millennium", Pisa, Italy, October 10-12, 1999.

MIUR “FIRB” (2012-2014).
Mitochondrial Ca2+ signalling plays pleiotropic roles, e.g. stimulation of aerobic metabolism and ATP production, buffering of cytosolic Ca2+ transients,regulation of cell fate. We are interested in dissecting the physiopathological outcomes of modulation of mitochondrial Ca2+ signalling. Accordingly, we focus our reasearch in two main areas: skeletal muscle homeostasis and triple negative breast cancer metastasis.
Rizzuto R, De Stefani D, Raffaello A, Mammucari C. (2012) Mitochondria as sensors and regulators of calcium signalling. Nat Rev Mol Cell Biol Aug 1;13(9):566-78.
Schiaffino S, Mammucari C.(2011) Regulation of skeletal muscle growth by the IGF1-Akt/PKB pathway: insights from genetic models. Skeletal Muscle Jan 24;1(1):4
Mammucari C, Patron M, Granatiero V, Rizzuto R. (2011) Molecules and roles of mitochondrial calcium signaling. Biofactors May-June;37(3):219-27
Mammucari C, Rizzuto R. (2010) Signaling pathways in mitochondrial dysfunction and aging. Mech Ageing Dev. Jul-Aug;131(7-8):536-43
Rossi AC, Mammucari C, Argentini C, Reggiani C, Schiaffino S. (2010) Two novel/ancient myosins in mammalian skeletal muscles: MYH14/7b and MYH15 are expressed in extraocular muscles and muscle spindles. J Physiol. Jan 15;588(Pt 2):353-64.
Masiero E, Agatea L, Mammucari C, Blaauw B, Loro E, Komatsu M, Metzger D, Reggiani C, Schiaffino S, Sandri M.(2009) Autophagy is required to maintain muscle mass. Cell Metab. Dec;10(6):507-15.
Blaauw B, Canato M, Agatea L, Toniolo L, Mammucari C, Masiero E, Abraham R, Sandri M, Schiaffino S, Reggiani C. (2009) Inducible activation of Akt increases skeletal muscle mass and force without satellite cell activation. FASEB J. Nov;23(11):3896-905.
Sartori R, Milan G, Patron M, Mammucari C, Blaauw B, Abraham R, Sandri M.(2009 Smad2 and 3 transcription factors control muscle mass in adulthood. Am J Physiol Cell Physiol. Jun;296(6):C1248-57. Epub 2009 Apr 8.
Dobrowolny G., Aucello M., Rizzuto E., Beccafico S., Mammucari C., Bonconpagni S., Belia S., Wannenes F., Nicoletti C., Del Prete Z., Rosenthal N., Molinaro M., Protasi F., Fanò G., Sandri M., Musarò A.,(2008 Skeletal muscle is a primary target of SOD1G93A-mediated toxicity. Cell Metab. Nov;8(5):425-36.
Blaauw B., Mammucari C., Toniolo L., Agatea L., Abraham R., Sandri M., Reggiani C., Schiaffino S.,(2008) Akt activation prevents the force drop induced by eccentric contractions in dystrophin-deficient skeletal muscle. Hum Mol Genet. Aug 27.
Schiaffino S., Mammucari C., and Sandri M.(2008) The role of autophagy in neonatal tissues. Autophagy June 1; 4:5, 727-730.
Mammucari C., Schiaffino S., Sandri M..(2008) Downstream of Akt: mTOR and FoxO3 in the regulation of autophagy in skeletal muscle. Autophagy May 16; 4:4, 524-526.
Mammucari C., Milan G., Romanello V., Rudolph R., Masiero E., Del Piccolo P., Burden S.J., Di Lisi R., Sandri C., Schiaffino S., Sandri M.(2007) FoxO3 controls autophagy in skeletal muscle in vivo. Cell Metab. Dec;6:458-71.
Project Title:
The role of mitochondrial calcium signalling in skeletal muscle trophism
Skeletal muscle atrophy is due to a number of causes, e.g. disuse, denervation, aging, fasting and cancer cachexia. In recent years, lots of efforts have been made to understand the molecular pathways, and thus the potential therapeutic targets, of muscle atrophy.
Mitochondria play a central role in skeletal muscle homeostasis, being the major source of ATP in oxidative myofibers. They have the ability to accumulate Ca2+, behaving as buffers of the cytosolic [Ca2+] increase occurring during contraction. In addition, mitochondrial Ca2+ stimulates aerobic metabolism, and thus ATP production, essential for muscle activity. Finally, excessive Ca2+ accumulation in mitochondria can trigger cell death.
The recent molecular identification of the Mitochondrial Calcium Uniporter (MCU), the highly selective channel responsible for Ca2+ entry into the mitochondria, has paved the way to novel experimental approaches, in which mitochondrial Ca2+ accumulation can be tightly regulated. Moreover, direct measurement and modulation of MCU expression and activity in different physiopathological conditions can now be performed.