Dario Diviani group


 

Heart failure is a chronic and lethal syndrome leads to a progressive decrease in cardiac function. In industrialized countries, it affects 10% of the population aged 65 and over. In the final stages of the disease cardiac output is no longer sufficient to match the oxygen and metabolic needs of the body, resulting in organ failure and death. A number of stresses and insults can trigger heart failure including long-term hypertension, myocardial infarction (MI), excess production of hormones and neurotransmitters, as well as exposure to drugs and toxicants. Ventricular cardiomyocytes initially adapt to the increased workload imposed by these cardiac insults by hypertrophying. While this compensatory process initially reduces the stress on ventricular walls and normalizes cardiac output, on the long term it predisposes to adverse ventricular remodeling associated with cardiomyocyte apoptosis, interstitial fibrosis, and impaired cardiac function.

Our laboratory investigates a range of focus areas, all of which center on understanding the molecular mechanisms governing heart dysfunction and repair. We have shown that the intracellular transduction events controlling these processes are regulated by scaffolding and anchoring proteins, which ensure coordination of signals in space and time. In particular, A-kinase anchoring proteins (AKAPs), assemble multifunctional signaling complexes that orchestrate and synchronize cellular processes associated with cardiac remodeling and protection.

 

 

Presentation_Figure 1_DD.png

Schematic representation illustrating the cardiac remodeling process induced by various pathological stresses.

 

D_Diviani_01.2020-1.jpg

Dario Diviani

Group leader

+41 21 692 53 80

dario.diviani@unil.ch

Rue du Bugnon 7 - CH-1005 Lausanne
Switzerland
Tel. +41 21 692 55 00
Fax +41 21 692 55 05