How is mitochondrial form-function relationship established?
What is its role in cell signalling and in age-associated diseases?

Mitochondria are crucial organelles in cell life and death: they synthetize most of cellular ATP, integrate signalling pathways and amplify cell death. This versatility is mirrored by their dynamic morphology, ultrastructure and juxtaposition to the endoplasmic reticulum, all controlled by a set of “mitochondria-shaping proteins”. We are interested in understanding the mitochondrial form-function relationship in health and disease. We use an integrated approach of genetics, advanced imaging, biochemistry, physiology and electron tomography to unravel the role of mitochondrial dynamics in signalling and in complex cellular responses.

Besides being crucial organelles in ATP synthesis, mitochondria control multiple signaling cascades, amplify cell death and participate in a plethora of diseases ranging from genetic conditions to the diseases of ageing that we study at VIMM. Mitochondrial function and dysfunction are mirrored by shape changes, controlled by a small set of mitochondria-shaping proteins that include Optic atrophy 1 (Opa1), Mitofusins (Mfn) 1&2, Dynamin related protein 1 (Drp1), Mitochondrial fission factor (Mff), Mitochondrial Dynamics (MiD)49&51, Fission 1 (Fis1).

The Scorrano lab has changed classical tenets in the field of apoptosis and mitochondrial pathophysiology and propelled the fields of mitochondrial dynamics and interorganellar contact sites. His lab discovered the Opa1-dependent “molecular staple” holding cristae junctions tight and exploited it in vivo to correct mitochondrial diseases and blunt muscular atrophy, stroke and heart ischemia; identified Mfn2, mutated in a peripheral neuropathy as the first molecular bridge between endoplasmic reticulum and mitochondria; understood how mitochondrial shape controls the outcome of autophagy; defined the molecular link between cristae shape, cellular respiration and growth; identified the essential role of mitochondrial fusion in heart development. We now wish to understand the molecular mechanisms and pathophysiological consequences of mitochondrial shape changes and contacts with the ER in health and in diseases associated to ageing.

Luca Scorrano


  • MD: University of Padova Medical School, Italy (1996)
  • PhD: Dept. of Biomedical Sciences, University of Padova (2000)
  • Postdoc: Dana-Farber Cancer Institute, Harvard Medical School, Boston, USA (2000-2003)
  • Group leader: Assistant Telethon Scientist, Dulbecco-Telethon Institute, Venetian Institute of Molecular Medicine, Padova, Italy (2003-2006)
  • Professor: Dept. of Physiology and Metabolism, University of Geneva Medical School, Geneva (Switzerland) (2007-2013)
  • Professor of Biochemistry, Dept. of Biology, University of Padova (since 2013)
  • Scientific Director, VIMM (since 2014)

Selected Awards

  • Elected Member, Academia Europaea, Section of Biochemistry and Molecular Biology (2019)
  • ESCI Award for Excellence in Basic/Translational Research, European Society for Clinical Investigation (2013)
  • Elected Member, EMBO (2012)
  • Eppendorf European Young Investigator Award, Eppendorf-Nature (2006)
  • EMBO Young Investigator (2006)

Current funding

  • MDA
  • Fondazione Telethon
  • AFM Telethon
  • Fondazione AIRC