MYOPHAGY

DEFINING THE MECHANISMS OF AGE-RELATED MUSCLE LOSS: FOCUS ON AUTOPHAGY

 Coordinatore FONDAZIONE PER LA RICERCA BIOMEDICA AVANZATA ONLUS 

Spiacenti, non ci sono informazioni su questo coordinatore. Contattare Fabio per maggiori infomrazioni, grazie.

 Nazionalità Coordinatore Italy [IT]
 Totale costo 1˙250˙000 €
 EC contributo 1˙250˙000 €
 Programma FP7-IDEAS-ERC
Specific programme: "Ideas" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013)
 Code Call ERC-2011-StG_20101109
 Funding Scheme ERC-SG
 Anno di inizio 2011
 Periodo (anno-mese-giorno) 2011-11-01   -   2016-10-31

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    FONDAZIONE PER LA RICERCA BIOMEDICA AVANZATA ONLUS

 Organization address address: Via Orus Giuseppe 2
city: PADOVA
postcode: 35129

contact info
Titolo: Ms.
Nome: Elena
Cognome: Grifalconi
Email: send email
Telefono: 390498000000
Fax: 390498000000

IT (PADOVA) hostInstitution 1˙250˙000.00
2    FONDAZIONE PER LA RICERCA BIOMEDICA AVANZATA ONLUS

 Organization address address: Via Orus Giuseppe 2
city: PADOVA
postcode: 35129

contact info
Titolo: Prof.
Nome: Marco
Cognome: Sandri
Email: send email
Telefono: +39 049 7923258
Fax: +39 049 7923250

IT (PADOVA) hostInstitution 1˙250˙000.00

Mappa


 Word cloud

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regulation    ageing    cross    activation    pathways    proteins    organelles    progressive    accident    muscle    proteasome    age    talk    sarcopenia    mass    autophagy    mechanisms    lysosome    loss    skeletal    weakness    ubiquitin    atrophy   

 Obiettivo del progetto (Objective)

'Muscle loss occurs in many diseases including cancer, AIDS, diabetes, renal or cardiac failure and sepsis. The wasting of muscle mass is characterized by the activation of an atrophy program that coordinates the ubiquitin-proteasome and autophagy-lysosome systems. The simultaneous activation of these systems allows the breakdown of contractile proteins and the removal of organelles. Ageing sarcopenia and frailty are also characterised by progressive muscle loss. However, the mechanisms that are at the base of this weakness are obscure. Sarcopenia results in a progressive loss of mobility that decreases the quality of life and has major economic and social consequences. In fact the age-dependent muscle atrophy favour traumatic events, accident, fracture or illness which lead to aged person to become hospitalised and bed-ridden or housebound, thus -having a high mortality in the year following their accident. The signalling pathways, which regulate loss of proteins and organelles in muscle fibers, are just at the beginning to be understood. We have recently found that autophagy-lysosome system is critical to maintain muscle mass and that its alteration leads to muscle atrophy, weakness and to several features that are present in ageing sarcopenia. Thus, dissecting the regulation of autophagy system in skeletal muscle and its role in muscle homeostasis is crucial for developing new therapeutic tools to counteract sarcopenia. This project is an effort in this direction. We aim: i) to identify molecular mechanisms and pathways which are responsible for autophagy regulation in skeletal muscle and which may be targeted to combat age related muscle weakness, (ii) to dissect the cross-talk between muscle and nerve, (iii) to determine the cross-talk between autophagy-lysosome and ubiquitin-proteasome, iv) to translate the findings obtained in animal models to human skeletal muscles.'

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