Kevin A. Murach

The paper shows that exercise preconditioning enhances skeletal muscle hypertrophy through epigenetic and metabolic changes, specifically involving Smox and Wnt signaling.

The paper identifies age-related differences in the transcriptional states of MuSC-derived myonuclei in response to mechanical overload.

This study investigates the origin and dynamics of displaced myonuclei in skeletal muscle after injury, finding that non-satellite cell-derived myonuclei contribute significantly to muscle repair.

The paper shows that transient MYC activation in skeletal muscle mimics exercise-induced adaptations, leading to hypertrophy, metabolic changes, and fiber type shifts.

This study shows that myonuclear loss, not senescent myonuclei, is linked to fast fiber atrophy in aging human skeletal muscle.

The paper investigates the origin of displaced myonuclei in adult skeletal muscle, finding that both resident myonuclear migration and stem cell fusion contribute, depending on mechanical loading duration and fibre characteristics.

This study examines age-related differences in myonuclear multi-omic responses to muscle hypertrophy in mice, identifying transcriptional, epigenetic, and regulatory mechanisms underlying age-dependent muscle plasticity.

This study shows miR-1 regulates metabolic flexibility in skeletal muscle by controlling pyruvate metabolism, with loss of miR-1 causing metabolic inflexibility and reduced endurance.

This study maps the 24-hour molecular response to resistance exercise in human muscle, identifying MYC as a key regulator of hypertrophy and mRNA levels.

This study evaluates CRISPR-based gene integration in skeletal muscle using two high-expressing loci, demonstrating high-level therapeutic gene expression in mouse myoblasts.

This paper introduces a novel mouse model of ovarian cancer cachexia showing that muscle weakness and mitochondrial stress occur before metastasis and atrophy in specific muscles.

This study identifies biphasic transcriptional changes in female skeletal muscle during cancer cachexia, distinct from males, with sex-specific gene expression patterns and implications for therapeutic targets.