Abstract
Myopathies constitute a heterogeneous group of disorders defined by impaired skeletal muscle functions that originate from structural, metabolic, genetic, or inflammatory abnormalities. At the biochemical level, these conditions are characterized by significant disruptions in essential processes, including energy metabolism, calcium homeostasis, and redox balance. For instance, defects in pathways such as glycolysis, fatty acid oxidation, and mitochondrial oxidative phosphorylation severely restrict ATP production, resulting in muscle fatigue, while the concurrent elevation of reactive oxygen species (ROS) triggers oxidative damage and accelerates disease progression. Recent advances in molecular biology have considerably deepened our understanding of the genetic and biochemical mechanisms that drive myopathies, consequently facilitating the development of targeted therapeutic interventions. Current interventions, ranging from antioxidant therapy and metabolic supplementation to gene therapy and enzyme replacement, strive to restore cellular function and decelerate the clinical course. This commentary examines the biochemical foundations of myopathies and critically evaluates emerging strategies for their effective remediation.
Keywords
Myopathy, Oxidative stress, Mitochondrial dysfunction, Calcium homeostasis, Gene therapy, Apoptosis, Necrosis, Autophagy