The autonomic nervous system continuosly adjusts cardiac activity to the needs of the body in the different environmental conditions, from rest to acute stresses.
i) How do sympathetic neurons communicate to cardiac cells to achieve flexible and reliable control over heart function?
ii) How does intercellular communication operate in diseases characterized (e.g. Heart Failure, Myocardial Infarction) dysfunction of the neurogenic control of the heart?

The lab is devoted to improving basic understanding of cardiac cell biology and the mechanisms of neurogenic regulation of cardiac function. In particular we focus on the biophysics of intercellular communication between autonomic neurons and cardioimyocytes, and how alterations in this process may underlie stress-dependent arryhthmias and heart failure. The lab employs techniques ranging from molecular and cell biology, to advanced fluorescence based measurements of second messenger dynamics, to optogenetics.

The sympathetic nervous system is an important physiologic modulator of the heart. Sympathetic neurons play a critical role in matching cardiac function with the acute variation of perfusional requests, as those associated to changes in somatic activity or emotions; in addition, they adapt myocardial structure to states of chronically elevated workload, such as hypertension or valvular diseases.
Extensive research has led to the common tenet that sympathetic innervation controls cardiac function and structure by releasing neurotransmitters (mainly noradrenaline) into the heart interstitium, causing activation of adrenergic receptors in the target cells.
We have previously demonstrated that the myocardial sympathetic network is highly organized and the neuro-cardiac interaction is underain by multiple interaction sites bringing neurons at very narrow intercellular distance with the target cardiomyocyte membrane. Based on this finding, our research aim is to understand the biophysics of neuro-cardiac communication in the physiological heart and in diseases associated to dysfunctional autonomic cardiac innervation.
A well determined condition leading to the development of arrhythmia in structrurally intact hearts is unbalanced activation of the sympathetic neurons in different regions of the heart. We aim to test whether dysregulation of neuro-effector mechanisms may feature in common genetic arrhythmia syndromes, e.g. Catecholaminergic Polymorphic Ventricular Tachycardia (CPVT).

MARCO MONGILLO

  • 2015 – present Associate Professor, Dept of Biomedical Sciences, University of Padua
  • 2009 – present PI, Venetian Institute of Molecular Medicine, Padua
  • 2008 – 2015 Researcher at the Faculty of Medicine, University of Padua
  • 2006 – 2008 Research Fellowship, Columbia University, New York
  • 2005 – 2006 Clinical Fellow, Imperial College London, UK
  • 2005 Ph.D. in Molecular and Cellular Biology and Pathology, University of Padua
  • 2001 Degree in Medicine at the University of Padua

Selected Awards

  • 2005 – Bocchetti Protti Award, Belluno, Italy
  • 2006 – Norman Alpert Award, European Society of Cardiology
  • 2016 – Guido Tarone Award, Heart Failure Association of the ESC