BIOM30001 Lecture Notes - Lecture 22: Skeletal Muscle, Myod, Sarcolemma
Document Summary
Catabolic factors (muscle disuse, glucocorticoids, ros, systemic inflammation) increases activity of this ubiquitin-proteasome pathway. Tnfa activates nfkb which inhibits myod which is an important myogenic regulatory factor. Required for activation, proliferation and differentiation of satellite cells (like stem cells, under sarcolemma, involved in regeneration/repair of skeletal muscle) Anabolic factors are decreased: insulin like growth factor (igf) is important for protein synthesis. It inhibits the ubiquitin-proteasome pathway and stimulates satellite cells. Stable patients have normal igf levels, but decline during exacerbations > increased wasting. Myostatin: a negative regulator of skeletal muscle growth. Part of tgfb superfamily, almost exclusively produced by skeletal muscle. Myostatin loss of function mutation causes a "double muscle" phenotype. Myostatin inhibits activation/proliferation/differentiation of satellite cells into muscle fibres. Can form new myofibres or can attach to damaged myofibre and repair it. Myostatin mrna expression correlates with bmi during aecopd but not in stable copd.
