NF-kappa-B Contributes To Muscle Wasting

Main Category: Genetics
Also Included In: Muscular Dystrophy / ALS;  Cancer / Oncology
Article Date: 06 Nov 2006 - 3:00 PDT

email to a friend   printer friendly   opinions  

Muscle wasting is a widespread problem for individuals of all ages. It can be caused by genetic defects, such as the genetic defect that causes Duchenne muscular dystrophy, as well as be a secondary consequence of other diseases, such as cancer and diseases of the immune system. However, the molecular events that lead to muscle wasting are not well defined, meaning that treatments for this disease have not been developed.

Now, in a study appearing in the November issue of the Journal of Clinical Investigation, Foteini Mourkioti and colleagues at the European Molecular Biology Laboratory (EMBL) Mouse Biology Unit in Monterotondo-Scalo, Italy, have shown that the muscles of mice lacking the protein IKK2 (which is required for activation of a regulator of gene expression NF-kappa-B) in muscle cells were stronger than the muscles of normal mice. Furthermore, mice lacking IKK2 in muscle cells were protected against muscle wasting caused by either denervation or exposure to a toxin. These data indicate that IKK2 activation of NF-kappa-B is one molecular pathway that leads to muscle wasting and cause the authors to suggest that agents targeting this pathway might have potential as therapeutics for the treatment of muscle wasting

In an accompanying commentary, Michael Karin -- from the University of California San Diego -- suggests that because NF-kappa-B is a key regulator of gene expression during inflammation, inflammation might have a pathogenic role in muscle degenerative disease and that anti-inflammatory therapies might prove beneficial to individuals with such diseases.

TITLE: Targeted ablation of IKK2 improves skeletal muscle strength, maintains mass, and promotes regeneration

AUTHOR CONTACT:

Foteini Mourkioti
European Molecular Biology Laboratory (EMBL) Mouse Biology Unit, Monterotondo-Scalo, Italy.

Anna-Lynn Wegener
Press Officer
EMBL, Heidelberg, Germany

ACCOMPANYING COMMENTARY

TITLE: Role for IKK2 in muscle: waste not, want not

AUTHOR CONTACT:

Michael Karin
University of California San Diego, La Jolla, California, USA.

###

Contact: Karen Honey
Journal of Clinical Investigation

• Additional
• References
• Citations