Marine Theret

AMPKα1-LDHA, a new metabolic pathway, regulating stem cell fate.

Analysis of Muscle Stem Cell Fate Through Modulation of AMPK Activity.

The origins and non-canonical functions of macrophages in development and regeneration.

Cross-talk between TGF-β and PDGFRα signaling pathways regulates the fate of stromal fibro-adipogenic progenitors.

TGF-β-driven downregulation of the transcription factor TCF7L2 affects Wnt/β-catenin signaling in PDGFRα fibroblasts.

High prevalence of plasma lipid abnormalities in human and canine Duchenne and Becker muscular dystrophies depicts a new type of primary genetic dyslipidemia.

In vitro assessment of anti-fibrotic drug activity does not predict in vivo efficacy in murine models of Duchenne muscular dystrophy.

Evolving Roles of Muscle-Resident Fibro-Adipogenic Progenitors in Health, Regeneration, Neuromuscular Disorders, and Aging.

The Effect of Posterior Lumbar Spinal Surgery on Biomechanical Properties of Rat Paraspinal Muscles 13 Weeks After Surgery.

Origins, potency, and heterogeneity of skeletal muscle fibro-adipogenic progenitors-time for new definitions.

Larger muscle fibers and fiber bundles manifest smaller elastic modulus in paraspinal muscles of rats and humans.

Macrophages in Skeletal Muscle Dystrophies, An Entangled Partner.

Multipotent stromal cells: One name, multiple identities.

Cholesterol absorption blocker ezetimibe prevents muscle wasting in severe dysferlin-deficient and mdx mice.

Elevated numbers of infiltrating eosinophils accelerate the progression of Duchenne muscular dystrophy pathology in mdx mice.

Pleiotropic activation of endothelial function by angiotensin II receptor blockers is crucial to their protective anti-vascular remodeling effects.

Thermoneutral Housing and a Western Diet Combination Exacerbates Dysferlin-Deficient Muscular Dystrophy.

Spatial compartmentalization of signaling imparts source-specific functions on secreted factors.

Origins and functions of eosinophils in two non-mucosal tissues.

Skeletal muscle niche, at the crossroad of cell/cell communications.

Apolipoprotein E knockout, but not cholesteryl ester transfer protein (CETP)-associated high-density lipoprotein cholesterol (HDL-C) lowering, exacerbates muscle wasting in dysferlin-null mice.