Gene-based interventions, including antioxidant gene delivery, Nrf2 activation, RNA modulators, and CRISPR editing, offer new avenues but remain limited by safety and delivery barriers.
First-pass extracted concept
gene-based interventions for skeletal muscle atrophy
Aliases
antioxidant gene delivery, CRISPR editing, Nrf2 activation, RNA modulators
Evidence Snippets
Supporting Sources
Linked Claims
Neuromuscular junction destabilization, excitation-contraction coupling defects, and mitochondrial dysfunction intensify calcium dysregulation and promote reactive oxygen and nitrogen species accumulation in skeletal muscle atrophy.
Skeletal muscle atrophy emerges from intertwined neuromuscular and metabolic failures, in which neuromuscular junction destabilization, excitation contraction coupling defects, and mitochondrial dysfunction collectively intensify calcium dysregulation and drive the accumulation of reactive oxygen and nitrogen species (RONS)
RONS-mediated activation of NF-kB and FOXO pathways accelerates ubiquitin-proteasome and autophagy-lysosome degradation, contributing to motor unit loss.
RONS-mediated activation of NF-baB and FOXO pathways accelerates ubiquitin proteasome and autophagy lysosome degradation, leading to motor unit loss.
Gene-based interventions including antioxidant gene delivery, Nrf2 activation, RNA modulators, and CRISPR editing are promising for skeletal muscle atrophy but are limited by safety and delivery barriers.
Gene-based interventions, including antioxidant gene delivery, Nrf2 activation, RNA modulators, and CRISPR editing, offer new avenues but remain limited by safety and delivery barriers.
Translational progress in skeletal muscle atrophy therapy requires rigorous safety pipelines, mechanistic biomarkers of motor unit recovery, and modular combination regimens integrating cells, genes, scaffolds, and rehabilitative input.
Translational progress requires rigorous safety pipelines, mechanistic biomarkers of motor unit recovery, and modular combination regimens that integrate cells, genes, scaffolds, and rehabilitative input.