Research Group Jean-Paul Thissen

EDIN

Regulation of skeletal muscle mass by hormones

Towards new targets to mitigate muscle atrophy and new biomarkers for its diagnosis

Muscle atrophy, observed in catabolic states such as cancer cachexia, immobilization or aging is associated with muscle functional loss contributing to morbidity and mortality. Due to lack of effective treatments, new approaches have been actively investigated. Attention has been oriented towards the potential benefits of the Myostatin (Mstn) inhibition. This growth factor strongly inhibits the muscle mass development. Given its marked anabolic effect, Mstn inhibition appears as a promising way to treat muscle atrophy. The deciphering of the mechanisms by which Mstn inhibition stimulates muscle mass should provide critical information not only for understanding the control of muscle size in general but also for developing new therapeutic strategies.

Publications 2017-2018

Gueugneau, M. et al. (2018) Increased Serpina3n release into circulation during glucocorticoid-mediated muscle atrophy. J Cachexia Sarcopenia Muscle, in press.

Bindels, L. et al. (2018) Increased gut permeability in cancer cachexia: mechanisms and clinical relevance. Oncotarget 9: 18224-18238

Barbe C, Bray F, Gueugneau M, Devassine S, Lause P, Tokarski C, Rolando C, Thissen JP (2017) Comparative Proteomic and Transcriptomic Analysis of Follistatin-Induced Skeletal Muscle Hypertrophy. Journal of proteome research 16, 3477-3490

Loumaye A, de Barsy M, Nachit M, Lause P, van Maanen A, Trefois P, Gruson D, Thissen JP (2017) Circulating Activin A predicts survival in cancer patients. J Cachexia Sarcopenia Muscle 8, 768-777

Loumaye A, Thissen JP (2017) Biomarkers of cancer cachexia. Clin Biochem 50, 1281-1288