Adam Philip Sharples

This study shows repeated disuse atrophy creates a molecular memory in skeletal muscle, leading to transcriptional resilience in young adults but increased susceptibility in aged muscle.

This study investigates how UBR-box E3 ubiquitin ligases respond to changes in protein synthesis and skeletal muscle size, finding increased abundance and activity of these ligases under conditions of muscle growth and regeneration.

The paper creates a DNA methylation aging atlas across 17 human tissues, identifying conserved and tissue-specific aging signatures and potential therapeutic targets.

This study shows that resistance training induces reversible and retained proteomic changes in human skeletal muscle, suggesting a proteomic memory of muscle growth.

This study shows that human skeletal muscle retains epigenetic memory of high-intensity interval training (HIIT) through hypomethylation and increased gene expression even after detraining.

This study integrates multi-OMIC data from 12 cohorts to identify exercise-specific molecular signatures and gene regulatory patterns in human skeletal muscle.

This study shows exercise training reduces epigenetic and transcriptomic aging in human skeletal muscle, while muscle disuse accelerates transcriptomic aging.

This study compares DNA methylation and mRNA responses to lower- versus higher-load resistance exercise in trained men, finding similar gene expression and methylation patterns despite differences in exercise intensity.

Resistance training reduces methylation at 63% of mtDNA CpG sites in older males, mimicking a youthful methylome signature and enhancing mitochondrial function.

The paper identifies age-related DNA methylation changes in human skeletal muscle through a meta-analysis and integrates these with transcriptomic and proteomic data, revealing enriched age-related gene expression patterns.

The paper develops a muscle-specific epigenetic clock using DNA methylation data from skeletal muscle samples, achieving higher accuracy than a pan-tissue clock.