Cachexia; Cancer; Sarcopenia Clinical Trial
Official title:
The Role of the Muscle-nervous System Interface in Cancer Cachexia
Sarcopenia is an important component of cachexia associated with cancer, and their high incidence in cancer patients emphasizes the need for a better understanding of its mechanisms, which can result in better therapeutic interventions to reverse this situation and improve the prognosis. Our hypothesis is that the plasma concentration of IL-6 and c-terminal agrin is directly correlated with the loss of muscle mass and development of cachexia.
The agrin is a protein that acts on neuromuscular junctions (NMJs) promoting stabilization of
same, which results in the maintenance and growth of muscle fibers, but the cleavage of
agrin, a process by which is formed the agrin fragment C-terminus (CAF), has been linked to
the development of sarcopenia, because its presence is directly linked to the reduction in
the number of muscle fibers, increasing the heterogeneity of fiber size, presence of Central
cores and increasing the proportion of type I fibers and consequently a greater degradation
of lean body mass. Studies in mice show that the greatest cleavage of agrin carries on
development of sarcopenia and human studies report that individuals with higher serum levels
of sarcopenia CAF compared to individuals without sarcopenia.
Therefore, aiming at the complexity of cancer associated with the cachexia and the great
importance of the maintenance of lean body mass to a better prognosis in disease, is of
fundamental importance to elucidate the role of CAF and the factors associated with
sarcopenia, the possible use of these proteins for diagnosis and the contribution that this
clarification could bring in clinical therapy.
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