Oct 2012 - present: Research Scientist, Neuroscience Institute, National Research Council of Italy (CNR), Padova, Italy.

2010 – 2012: Postdoctoral Fellow, Department of Biomedical Sciences, University of Padova, Italy.
2008 – 2010: Postdoctoral Fellow, Division of Cardiology, Johns Hopkins Medical Institutions, Baltimore, MD, USA.
2005 - 2008: PhD in Biochemistry and Biophysics, University of Padova, Italy.

Monoamine oxidase involvement in oxidative stress and mitochondrial dysfunction in cardiovascular diseases
Identification of the important sources of reactive oxygen species (ROS) in the cell is of major importance, since cardiac tissue redox balance plays a major role in myocyte hypertrophy and failure. Within the mitochondria, monoamine oxidases (MAO) have been demonstrated to generate large amounts of ROS. These flavoenzymes are localized at the level of the outer mitochondrial membrane and exist in two isoforms, MAO-A and –B and are responsible for the catabolism of neurotransmitters and biogenic amines, generating hydrogen peroxide during this process.
Previous work from our group showed that both MAO isoforms play a central role in maladaptive hypertrophy and heart failure through enhanced catecholamine catabolism, resulting in increased oxidative stress, apoptosis and cardiac dysfunction. Importantly, both pharmacological and genetic inhibition of these enzymes prevents the transition of concentric, compensated hypertrophy to heart failure. Using redox sensitive probes targeted specifically to mitochondria or to the cytosol, we showed that MAO activation results in H2O2 generation predominantly in the mitochondria, leading eventually to mitochondrial dysfunction.
Currently I am investigating the role of MAOs in diabetic cardiomyopathy, how post-translational changes of MAO protein may impact its activity and how cellular and mitochondrial redox state might regulate protein expression.

  1. Kaludercic N, Mialet-Perez J, Paolocci N, Parini A, Di Lisa F: Monoamine oxidases as sources of oxidants in the heart. J Mol Cell Cardiol, 2014 Jan 9.
  2. Kaludercic N, Carpi A, Nagayama T, Sivakumaran V, Zhu G, Lai EW, Bedja D, De Mario A, Chen K, Gabrielson KL, Lindsey ML, Pacak K, Takimoto E, Shih JC, Kass DA, Di Lisa F, Paolocci N: Monoamine Oxidase B Prompts Mitochondrial and Cardiac Dysfunction in Pressure Overloaded Hearts. Antioxid Redox Signal. 2014 Jan 10;20(2):267-80.
  3. Kaludercic N, Takimoto E, Nagayama T, Lai EW, Feng N, Bedja D, Shih JC, Chen K, Gabrielson KL, Pacak K, Blakely RD, Kass DA, Di Lisa F, Paolocci N: Monoamine oxidase A mediated enhanced catabolism of norepinephrine contributes to adverse remodeling and pump failure in hearts with pressure overload. Circ Res. 2010 Jan 8;106(1):193-202.
  4. Agnetti G, Kaludercic N, Kane L, Elliott ST, Guo Y, Chakir K, Samantapudi D, Paolocci N, Tomaselli GF, Kass DA, Van Eyk JE: Modulation of mitochondrial proteome and improved mitochondrial function by biventricular pacing of dyssynchronous failing hearts. Circ Cardiovasc Genet. 2010 Feb 1;3(1):78-87.
  5. Kaludercic N, Carpi A, Menabò R, Di Lisa F, Paolocci N: Monoamine oxidases (MAO) in the pathogenesis of heart failure and ischemia/reperfusion injury. Biochim Biophys Acta. 2010 Sep 24.

2014-2016    EFSD/Sanofi European Research Programme: Innovative Approaches for the Treatment of Type 1 and Type 2 Diabetes.
2008-2010    American Heart Association Post-doctoral Grant Award for the 2-year project: “Monoamine oxidases (MAO) in hypertrophy and heart failure.”