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Helping muscle regenerate

Muscle wasting can occur at all ages as the result of genetic defects, heart failure, spinal injury or cancer. A therapy to cure the loss of muscle mass and strength, which has a severe impact on patients' lives, is desperately sought. Blocking a central signal molecule, researchers from the Mouse Biology Unit of the European Molecular Biology Laboratory (EMBL) in Monterotondo, Italy, have now found a way to protect muscle from degenerating after injury and to improve muscle healing in mice. The study appears in the current issue of the Journal of Clinical Investigation and suggests two molecules with the potential to speed up the regeneration of damaged muscle as promising drug targets for new therapies against muscle wasting.

We don't realise it when it is working fine, but our muscle is an intricate system that depends on a well regulated balance of protein production and breakdown. When this balance gets disturbed by disease or injury our muscles fade away, and with them our strength. A crucial player in this process is the signalling molecule NF-kB. It is well known as a messenger of inflammation and has recently been implicated in other degenerative conditions such as multiple sclerosis. The groups of Nadia Rosenthal and Manolis Pasparakis at the EMBL Mouse Biology Unit have now investigated the role NF-kB plays in muscle wasting.

First, they genetically removed NF-kB from the leg muscles of mice by blocking IKK2, a protein needed to activate the signal. Then, to mimic spinal injury, they blocked the communication between the spinal cord and the lower leg muscle an intervention that under normal circumstances inevitably leads to muscle wasting.

"What we observed was truly amazing", says Rosenthal, Head of EMBL's Mouse Biology Unit. "The mice showed hardly any muscle wasting after the injury; their muscle fibres maintained almost the same size, strength and distribution as in a healthy muscle. But that's not all; blocking IKK2 also helped mu
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Contact: Anna-Lynn Wegener
wegener@embl.de
49-622-138-7452
European Molecular Biology Laboratory
1-Nov-2006


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