Estelle Trifilieff, PhD
Our research focusses on developing treatments for patients suffering from skeletal muscle wasting due to aging (sarcopenia), debilitating inherent muscular defects such as myopathies, or chronic diseases resulting in cachexia. Typically, the reduction in strength and physical capabilities associated with loss of muscle mass results in functional limitations, reduced quality of life, and increased mortality. We are exploring several components of skeletal muscle loss observed in multiple wasting conditions, including the imbalance between protein synthesis and degradation, the role of muscle stem cells and senescent cells, the reduction in metabolic capabilities, and the maintenance of the motor neuron junction, to name just a few. In skeletal muscle injury conditions, in aging, and in dystrophies, changes in tissue composition including fibrosis and fat infiltration have been observed and likely contribute to stiffness and reduced functional response; these changes occur alongside impairment in components such as neuromuscular junction and metabolic capability. Therefore, we wish to understand the influence of skeletal muscle adaptation on adipogenesis in the context of body composition. We aim to elucidate the role and contribution of various pathways to muscle wasting occurring in sarcopenia and in various diseases such as cachexia and dystrophies, among others. These new insights into pathogenesis will serve as a foundation for our drug development effort toward innovative therapies.
Treatment of sporadic inclusion body myositis with bimagrumab.
Amato AA, Sivakumar K, Goyal N, David WS, SalajeghenM, Praestgaard J, Lach-Trifilieff E, Trendelenburg AU, Laurent D, Glass DJ, Roubenoff R , Tseng BS, Greenberg SA
Neurology, 2014, 83:2239-46.
An antibody blocking activin type II receptors induces strong skeletal muscle hypertrophy and protects from atrophy.
Lach-Trifilieff E, Minetti GC, Sheppard K, Ibebunjo C, Feige JN, Hartmann S, Brachat S, Rivet H, Koelbing C, Morvan F, Hatakeyama S, Glass DJ.
Mol Cell Biol, 2014, 34:606-18.
Blockade of the activin receptor IIb activates functional brown adipogenesis and thermogenesis by inducing mitochondrial oxidative metabolism.
Fournier B, Murray B, Gutzwiller S, Marcaletti S, Marcellin D, Bergling S, Brachat S, Persohn E, Pierrel E, Bombard F, Hatakeyama S, Trendelenburg AU, Morvan F, Richardson B, Glass DJ, Lach-Trifilieff E, Feige JN.
Mol Cell Biol, 2012, 32:2871-9.
Click here for additional publications.