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Muscle myostatin signalling is enhanced in experimental cancer cachexia

Background/Aims   Myostatin belongs to the transforming growth factor‐β superfamily and negatively regulates skeletal muscle mass. Its deletion induces muscle overgrowth, while, on the contrary, its overexpression or systemic administration cause muscle atrophy. The present study was aimed at investigating whether muscle depletion as occurring in an experimental model of cancer cachexia, the rat bearing the Yoshida AH‐130 hepatoma, is associated with modulations of myostatin signalling and whether the cytokine tumour necrosis factor‐α may be relevant in this regard.