Agency: Cordis | Branch: H2020 | Program: MSCA-RISE | Phase: MSCA-RISE-2014 | Award Amount: 1.46M | Year: 2016
A diverse variety of medical or lifestyle conditions lead to a progressive loss of muscle force by functionally impairing myofibril contractility and causing ultimately myofibril loss. Major underlying risk factors of chronic muscle force loss are ageing, inactive lifestyles, and unbalanced nutrition. Together, these factors are predicted to lead to an endemic incidence of muscle weakness both in the developed countries. Clinical research on the mechanisms involved requires a multidisciplinary approach covering aspects of ageing, metabolism, and on the humoral cross-talk of muscle with other key organs including heart, liver, kidney, and lung. To achieve this, six European groups with complementary expertise in inter-organ-cross-talk during stress-induced secondary myopathies will team-up with a leading team in the U.S. with expertise in the translation of muscle research into therapeutic interventions, and with one team from South Africa with cutting-edge expertise in the regulation of regenerative capacities in muscle. Importantly, four SMEs will participate in this RISE network that provide expertise in early muscle disease detection, monitoring, and the developing preventive strategies: Their knowledge on muscle disease detection at early stages and their monitoring during interventions will promote translational innovation. To implement innovation and our joint research program, both early stage and advanced researchers will be seconded from the academic eight teams to these four SMEs and vice versa. Thereby, this RISE scheme will establish a long-term collaborative University-SME driven translational innovative research program innovation in our interdisciplinary field of growing socioeconomic medical importance.
Agency: Cordis | Branch: FP7 | Program: CP-IP | Phase: HEALTH-2007-2.4.5-10 | Award Amount: 14.99M | Year: 2009
Ageing of skeletal muscle results in a progressive loss of mobility that decreases the quality of life and has major economic and social consequences for society at large. Increasing muscle weakness is a major component of muscle ageing. In the elderly muscles become atrophic (loss in muscle mass) and weaker (loss in muscle force), more susceptible to damage and consequently regenerate and recover more slowly than was the case in their youth. The challenge for FP7 is to identify the relative importance of sarcopaenia, thus proposing standards to define healthy ageing in order to identify age-related muscle weakness; secondly to identify molecular pathways which may be targeted to combat normal age related muscle weakness, and thirdly to identify therapeutic strategies to prevent muscle loss and weakness and enhance recovery following injury or immobilisation. The approaches which we will take to understand and combat muscle weakness in the aged population and improve healthspan can be defined in several steps: the collection and collation of data and samples, the assessment of physiological and functional parameters, the understanding of the various biological mechanisms involved, leading through integration to the development of strategies and their translation for the general European population. In order to develop and propose the general public with efficient countermeasures, the consortium will integrate data from genetics and epidemiology, molecular and cellular biology, physiology, biomechanics, as well as clinical and public health aspects, to ensure optimal scientific synergy from the leading European specialists and companies.
Agency: Cordis | Branch: FP7 | Program: ERC-SG | Phase: ERC-SG-LS4 | Award Amount: 1.25M | Year: 2011
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.