PUBLICATIONS
Here are a few examples of our publications, collaborations, and discoveries.
Full list of publications can be found here.
Resolvin-D2 targets myogenic cells and improves muscle regeneration in Duchenne muscular dystrophy
Discovery of a new treatment targeting muscle stem cells that is more effective than the current gold-standard treatment for DMD (glucocorticoids)
An engineered multicellular stem cell niche for the 3D derivation of human myogenic progenitors from iPSCs
Description of an optimized 3D protocol to generate iPSC-derived myoblasts
Clearance of defective muscle stem cells by senolytics reduces the expression of SASP and restores myogenesis in myotonic dystrophy type 1
Discovery that muscle stem cells are defective in DM1 and could be targeted as a therapeutic approach.
Apelin stimulation of the vascular skeletal muscle stem cell niche enhances endogenous repair in dystrophic mice
Discovery showing the therapeutic potential of targeting the vascular niche and MuSC defects in muscular diseases
Biallelic variants in the transcription factor PAX7 are a new genetic cause of myopathy
Discovery of a new genetic myopathy (named MYOSCO) that reveals a new class of "muscle stem cell myopathies"
EGFR-Aurka Signaling Rescues Polarity and Regeneration Defects in Dystrophin-Deficient Muscle Stem Cells by Increasing Asymmetric Divisions
Discovery of new therapeutic approaches targeting defective muscle stem cells in DMD
Fibro-adipogenic progenitors in skeletal muscle homeostasis, regeneration and diseases
Comprehensive review on the key role of FAPs in skeletal muscle.
N-acetylneuraminate pyruvate lyase controls sialylation of muscle glycoproteins essential for muscle regeneration and function
Discovery of MuSC defects in metabolic myopathy
Dystrophin expression in muscle stem cells regulates their polarity and asymmetric division
Discovery that muscle stem cells are intrinsically defective in DMD
Transient neonatal exposure to hyperoxia, an experimental model of preterm birth, leads to skeletal muscle atrophy and fiber type switching
Discovery that environmental changes (transient hyperoxia) induce long-term muscle defects.
The adhesion G-protein-coupled receptor Gpr116 is essential to maintain the skeletal muscle stem cell pool
Discovery of a new receptor regulating muscle stem cell quiescence.
Inhibition of type I PRMTs reforms muscle stem cell identity enhancing their therapeutic capacity
Discovery that MuSC function can be regulated by protein arginine methyltransferases inhibitors