Posted: March 22, 2010 |
Cellular activity may hold the key to future treatments for muscle-wasting related to inactivity and chronic illnesses |
(Nanowerk News) The interaction of a cellular substance known as
TWEAK and a cellular receptor to which TWEAK is drawn, can hasten the
weakening of muscle that is caused by disuse, a common and potentially
deadly complication of many diseases, including heart disease, cystic
fibrosis and cancer.
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A team of researchers led by Ashok Kumar, Ph.D., of the University of
Louisville’s Department of Anatomical Sciences and Neurobiology, will
publish these findings in the March 22, 2010 issue of the Journal of
Cell Biology. The study was funded by the National Institutes of
Health.
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“This finding, related to the interaction between TWEAK and a
receptor called Fn14 is very important because it has implications for
potential drug therapies that might use this interaction as a target,”
Kumar said. “Muscle wasting is not only a concern related to many
chronic conditions, but it is a serious problem afflicting astronauts
who spend any length of time in space and often require physical
rehabilitation upon return.”
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Previously, Kumar and his team studied the activity of TWEAK and the
Fn14 receptor in mice and found that overexpression of TWEAK caused
increased muscle loss around the time the animals reached six months of
age. This finding coincides with what is commonly observed in humans
when muscle loss occurs, Kumar said. However, studying what was
happening at the cellular level within the animals’ muscle, the
researchers were able to identify the TWEAK/ Fn14 connection.
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“While TWEAK is always present, its receptor is not expressed in
adult skeletal muscle,” Kumar said. “Conditions of inactivity lead
to the expression of TWEAK receptor on muscle cells and subsequent
binding of TWEAK to the receptor hastens muscle loss. Future studies
will help to determine the full range of clinically relevant settings in
which the TWEAK/ Fn14 pathway is operative, and in which inhibition of
this pathway is sufficient to preserve functional muscle.”
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Muscle atrophy as a complication of illness can hasten death by
affecting a patient’s ability to fight infection and in some cases
rendering patients unable to eat or breathe on their own. It is
sometimes treated with steroids but there is currently no widely
accepted drug treatment for the condition, Kumar said.
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