The majority of cancers are associated to cachexia, a severe form of weight loss mostly accounted for by skeletal muscle wasting. Cancer patients are often treated with chemotherapy, whose side effects are at times neglected or underestimated. Paradoxically, chemotherapy itself can induce muscle wasting with severe, cancer-independent effects on muscle homeostasis.
Activin negatively affects muscle fibers and progenitor cells in aging (sarcopenia) and in chronic diseases characterized by severe muscle wasting (cachexia). High circulating activin levels predict poor survival in cancer patients. However, the relative impact of activin in mediating muscle atrophy and hampered homeostasis is still unknown.
Activin negatively affects muscle fibers and progenitor cells in aging (sarcopenia) and
in chronic diseases characterized by severe muscle wasting (cachexia). High circulating
activin levels predict poor survival in cancer patients. However, the relative impact of
activin in mediating muscle atrophy and hampered homeostasis is still unknown. To
directly assess the involvement of activin, and its physiological inhibitor follistatin, in
cancer-induced muscle atrophy, we cultured C2C12 myotubes in the absence or in
© Università degli Studi di Roma "La Sapienza" - Piazzale Aldo Moro 5, 00185 Roma
