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Redox mechanisms of muscle dysfunction in inflammatory disease
REID MB; ANDRADE FH; BALKE CW; ESSER KA
PHYS MED REHABIL CLIN N AM , 2005, vol. 16, n° 4, p. 925-949 Doc n°: 122159 Localisation : Documentation IRR Descripteurs : AB12 - PATHOLOGIE / ETUDES GENERALES / MUSCLES Oxidative stress is a major component of the pathology that affects striated muscle in a wide variety of inflammatory diseases. Under these conditions, muscle-derived ROS exceed the local buffering capacity of tissue antioxidants; this perturbs the regulation of contractile function and gene expression, leading to loss of function via two parallel and largely independent mechanisms. The underlying biology can be illustrated using four different pathologic settings. First, in cachexia, elevated levels of circulating cytokines (notably TNF-a and IL-1B) act via receptor-mediated mechanisms to stimulate ROS production within muscle fibers. The resulting increase in ROS levels activates redox-sensitive signal transduction pathways that involve NF-?B and p38 MAPK Langue : ANGLAIS |
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