Repair of injured skeletal muscle: a molecular approach.
We review cellular and molecular processes involved in injury and repair of skeletal muscle with regard to the amount and location of damage produced. Discussion is based on advances made by use of newer techniques, including immunochemistry, in situ hybridization, molecular biology, ultrastructural analysis, and cell culture. Damage and repair processes after eccentric work, stretch, overload, chronic stimulation, cold injury, and other models are discussed for cellular and molecular components. Hypertrophy or hyperplasia can occur under certain conditions. After injury, satellite cells are activated by growth factors. These cells can also be activated during fiber-type transformation, probably to provide necessary DNA content rather than to supply cells of a new lineage. Emphasis is given to myosin mRNA studied by in situ hybridization to localize subcellular distribution. Increases in mRNA concentration are found near nuclei in damaged regions and at the subcellular sites being repaired in the middle of skeletal muscle fibers or near the myotendon junction. The activation of genes for muscle regulatory factors during development is compared with their activation in regeneration and response to injury.
Russell
B
B
Department of Physiology, University of Illinois, Chicago 60680.
Dix
D J
DJ
Haller
D L
DL
Jacobs-El
J
J
D000818:Animals; D002455:Cell Division; D002467:Cell Nucleus / Q000378:metabolism; D015870:Gene Expression; D006801:Humans; D006965:Hyperplasia; D006984:Hypertrophy; D009124:Muscle Proteins / Q000502:physiology; D009132:Muscles / Q000378:metabolism / Q000473:pathology* / Q000502:physiology; D009218:Myosins / Q000235:genetics / Q000378:metabolism; D009693:Nucleic Acid Hybridization; D012333:RNA, Messenger / Q000378:metabolism
D009124:Muscle Proteins; D012333:RNA, Messenger; D009218:Myosins