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Our goal is to identify new functions for the cells located in the microenvironment of muscle cells beside their canonical properties (e.g., regulation of inflammation for macrophages, supply of oxygen and nutriments for vessel cells) and how muscle stem cells and myofibers are controlled by their closest environment in both normal and pathological contexts. The identification of new molecules or novel functions of already known pathways are the basis for expanding our current understanding about skeletal muscle homeostasis and its pathophysiology.

Stem cells are important in the maintenance and repair of many tissues all along the life span. It is the case in skeletal muscle, which presents high plasticity and regenerative properties to keep constant physiological parameters (homeostasis). Normal skeletal muscle mobilizes tissue-associated endogenous stem cells, mainly satellite cells, to repair damaged myofibers. Indeed, muscle stem cells sustain regeneration that is crucial for muscle homeostasis, as well as the self-renewal mechanisms that maintain their pool constant.

A key issue we address is the tissue environment in which muscle stem cells are activated. Environment plays important roles in the behavior of muscle stem cells and myogenic cells, although the mechanisms are poorly unknown. Various cell types in the vicinity of stem cells communicate with each other to correctly drive regeneration. We explore the roles of immune cells (inflammation), endothelial and peri-endothelial cells (angiogenesis) and interstitial cells (fibrosis) on myogenic cell fate in normal healthy regenerating muscle and during muscular dystrophies. Indeed, myopathies are characterized by the alteration in the environment of muscle stem cells, such as the presence of chronic inflammation and fibrosis, which are detrimental for both tissue repair and cell therapies.

Publications

2025
Ilaria Andreana, Ananga Ghosh, Mathieu Repellin, Anita Kneppers, Sabrina Ben Larbi, Federica Tifni, ..., Nanoparticle delivery of AMPK activator 991 prevents its toxicity and improves muscle homeostasis in Duchenne muscular dystrophy, Molecular Therapy - Methods and Clinical Development.
2025
Charline Jomard, Natacha Boyer, Aurélie Fessard, Bénédicte Chazaud, Julien Gondin, Effect of analgesic treatments on voluntary activity, mechanical sensitivity and muscle regeneration after cardiotoxin injection in mice, Sci Rep 2025 Jul; 15(1): 27921.
2025
Aurélie Fessard, Aliki Zavoriti, Natacha Boyer, Jules Guillemaud, Masoud Rahmati, Peggy del Carmine..., Neuromuscular electrical stimulation training induces myonuclear accretion and hypertrophy in mice without overt signs of muscle damage and regeneration, Skelet Muscle 2025 Feb; 15(1): 3.
2023
Davi a G Mázala, Ravi Hindupur, Young Jae Moon, Fatima Shaikh, Iteoluwakishi H Gamu, Dhruv Alladi, ..., Altered muscle niche contributes to myogenic deficit in the D2-mdx model of severe DMD, Cell Death Discovery.
2023
Clara Bernard, Charline Jomard, Bénédicte Chazaud, Julien Gondin, Kinetics of skeletal muscle regeneration after mild and severe muscle damage induced by electrically‐evoked lengthening contractions, FASEB Journal.
2022
Mathilde Mura, Michèle Weiss-Gayet, Nellie Della Schiava, Erica Chirico, Patrick Lermusiaux, Marie ..., Monocyte Phenotypes and Physical Activity in Patients with Carotid Atherosclerosis, Antioxidants.
2017
Saclier M, Theret M, Mounier R, Chazaud B, Effects of Macrophage Conditioned-Medium on Murine and Human Muscle Cells: Analysis of Proliferation, Differentiation, and Fusion., Methods Mol Biol 2017 ; 1556(): 317-327.
2016
Varga T, Mounier R, Patsalos A, Gogolák P, Peloquin M, Horvath A, Pap A, Daniel B, Nagy G, Pintye E..., Macrophage PPARγ, a Lipid Activated Transcription Factor Controls the Growth Factor GDF3 and Skeletal Muscle Regeneration., Immunity 2016 Nov; 45(5): 1038-1051.
2016
Weiss-Gayet M, Starck J, Chaabouni A, Chazaud B, Morlé F, Notch Stimulates Both Self-Renewal and Lineage Plasticity in a Subset of Murine CD9High Committed Megakaryocytic Progenitors., PLoS One 2016 ; 11(4): e0153860.