Dr. Michelangelo Campanella Royal Veterinary College, University of London – The European Neuroscience Institute at University College London

Campanella Michelangelo

  • Young Investigator

Metabolism in Brain Diseases

About Dr. Michelangelo Campanella

The core of our research focuses on the understanding of mitochondrial function, metabolism and quality control regulation in mammals and organism models such as the Zebrafish. The bulk of our research stands on two fundamental concepts associated with the biology of mitochondria lying at the basis of cellular health: energy and quality. Pathways and molecules that may concomitantly impinge on both these aspects are therefore object of our attention aiming to provide information on key aspects of normal and abnormal cell function. 

Mitochondria play a central role in the pathologies of the central nervous system associated to progressive and irreversible degeneration of tissues –especially in those ageing related. In the same way, given the constant evasion of programmed cell death and metabolic switch, mitochondria are central for cell development. There are two principal topics on which our research activity is based upon:
- The glycolytic driven metabolism and the reversion of the mitochondrial F1Fo-ATPsynthase in mammalian and non-mammalian neuronal cells physiopathology.
- The functional role of the mitochondrial Translocator Protein (mTSPO) in the upset of metabolism and self-conservation mechanisms guarding the brain cells integrity.

By these lines of research, we are forming a novel conceptual and experimental framework to a) characterize neglected regulatory pathways underlying cell physiology as well as the onset and progression of diseases with the goal to b) identify bio-markers for diagnostic purposes and c) molecular targets for therapeutic intervention.

For further information, please also see: http://www.rvc.ac.uk/about/our-people/michelangelo-campanella

5 Selected Publications

Severinatne M., Faccenda D., De Biase V., Campanella M. In Bcl-2 knock-down cells, PK11195 inhibits mitophagy targeting the F1Fo-ATPsynthase. Curr. Mol. Med., in press.

Faccenda D., Tan CH., Seraphim A., Duchen MR., Campanella M. (2013) IF1 limits the apoptotic-signalling cascade by preventing remodelling of mitochondria. Cell Death Differ., 20 (5) : 686-97.

Shah DI., Takahashi-Makise N., Cooney JD., Li L., Schultz IJ., Pierce EL., Narla A., Seguin A., Hattangadi SM., Medlock AE., Langer NB., Dailey TA., Hurst SN., Faccenda D., Wiwczar JM., Heggers SK., Vogin G., Chen W., Chen C., Campagna DR., Brugnara C., Zhou Y., Ebert BL., Danial NN., Fleming MD., Ward DM., Campanella M., Dailey HA., Kaplan J., Paw BH. (2012) Nature, 491 (7425) : 608-12.

Gastaldello A., Callaghan H., Gami P., Campanella M. (2010) Ca2+-dependent autophagy is enhanced by the pharmacological agent by pharmacological agent PK11195 in autophagy. Autophagy., 6 (5) : 607-13.

Campanella M., Casswell E., Chong S., Farah Z., Wieckowski MR., Abramov AY., Tinker A., Duchen MR. (2008) Regulation of mitochondrial structure and function by the F1Fo-ATPase inhibitor protein, IF1. Cell Metab., 8 (1) : 13-25.

Awards, Fellowships and Honours

2012            FP6 Marie Curie Fellow
2010            Tianjin University Award for Foreign Expert
2007            Selected Marie Curie Fellow to Attend The Lindau Meeting of Nobel Laureates
2005            EIF Marie Curie Actions
2005            The Royal Society/Accademia dei Lincei, Short-Term Fellowship
2004            EMBO Short-Term Fellowship (2004)

Technical Expertise

  • Mitochondrial physiology and pathology
  • Cell biology and signalling
  • Regulation of neuronal cell metabolism 
  • Molecular and cellular pharmacology
  • Autophagy molecular signalling
  • Confocal live cell imaging