Skeletal Muscle: Myogenesis & Myopathy

Voluntary movement, which is effected by skeletal muscle, contributes greatly to energy metabolism and its regulation via glucose uptake and storage by insulin. Complications from aging and metabolic diseases like diabetes and metabolic syndrome are a factor in muscle wasting (atrophy). However, recent research hypothesizes that metabolic defects in skeletal muscle contribute to the etiology of diabetes and metabolic syndrome, suggesting that skeletal muscle has a larger role in these disease states than initially expected. Large heterogeneous protein complexes, including titin or dystrophin facilitate muscle contraction by connecting the skeletal muscle cytoskeleton to the extracellular matrix. Muscular dystrophies arise from inherited mutations in the genes encoding components of these complexes, and gene expression changes disrupting their normal contractile function dysregulate signaling pathways that control muscle growth. Potential therapies for muscle wasting include generation of new muscle cells (myogenesis) or increasing the mass of current muscle cells (hypertrophy). Thus, muscle-specific biological and pathophysiological processes are interrelated and cannot be studied in isolation.

QIAGEN provides a broad range of assay technologies for skeletal muscle research that enables analysis of gene expression and regulation, epigenetic modification, genotyping, and signal transduction pathway activation. Solutions optimized for skeletal muscle studies include PCR array, miRNA, siRNA, mutation analysis, pathway reporter, chromatin IP, DNA methylation, and protein expression products.