Muscle atrophy
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2008-07-04T14:58:51Z
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'''Muscle atrophy''' refers to a decrease in the size of skeletal muscle, which occurs in a variety of settings. Atrophy may or may not be distinct from "[[sarcopenia]]", which is the loss of muscle seen in the aged.
When a muscle atrophies, it necessarily becomes weaker, since the ability to exert force is related to mass.
==Clinical settings of atrophy==
There are many diseases and conditions which cause a decrease in [[muscle]] mass, known as [[atrophy]], including: inactivity, as seen when a cast is put on a limb, or upon extended bedrest (which can occur during a prolonged illness); [[cachexia]] - which is a "body-wasting" syndrome that is a co-morbidity of [[cancer]] and [[Congestive Heart Failure]]; [[Chronic Obstructive Pulmonary Disease]]; burns, liver failure, etc. Other syndromes or conditions which can induce skeletal muscle atrophy are congestive heart disease, liver disease, and starvation.
==Other muscles diseases, distinct from atrophy==
During aging, there is a gradual decrease in the ability to maintain skeletal muscle function and mass. This condition is called "[[sarcopenia]]". The exact cause of [[sarcopenia]] is unknown, but it may be due to a combination of the gradual failure in the "[[satellite cells]]" which help to regenerate skeletal muscle fibers, and a decrease in sensitivity to or the availability of critical secreted [[growth factors]] which are necessary to maintain muscle mass and satellite cell survival.
In addition to the simple loss of muscle mass ([[atrophy]]), or the age-related decrease in muscle function ([[sarcopenia]]), there are other diseases which may be caused by structural defects in the muscle ([[muscular dystrophy]]), or by inflammatory reactions in the body directed against muscle (the myopathies).
==Pathophysiology==
Muscle atrophy occurs by a change in the normal balance between protein synthesis and protein degradation. During atrophy, there is a down-regulation of protein synthesis pathways, and an activation of protein breakdown pathways<ref>Sandri M. 2008. Signaling in Muscle Atrophy and Hypertrophy. Physiology 23: 160-170. </ref>. The particular protein degradation pathway which seems to be responsible for much of the muscle loss seen in a muscle undergoing atrophy is the "ATP-dependent, [[ubiquitin]]/[[proteasome]] pathway. In this system, particular proteins are targeted for destruction by the ligation of at least four copies of a small peptide called [[ubiquitin]] onto a substrate protein. When a substrate is thus "poly-ubiquitinated", it is targeted for destruction by the [[proteasome]]. Particular enzymes in the ubiquitin/proteasome pathway allow ubiquitination to be directed to some proteins but not others - specificity is gained by coupling targeted proteins to an "E3 [[ubiquitin ligase]]". Each E3 [[ubiquitin ligase]] binds to a particular set of substrates, causing their ubiquitination.
==Potential treatment==
Muscle atrophy can be opposed by the signaling pathways which induce muscle hypertrophy, or an increase in muscle size. Therefore one way in which [[exercise]] induces an increase in muscle mass is to downregulate the pathways which have the opposite effect.
==See also==
*[[Muscle weakness]]
*[[Muscular dystrophy]]
*[[Myotonic dystrophy]]
==References==
<references/>
==External links==
* {{MeshName|Muscular+atrophy}}
[[Category:Physiology]]
[[Category:Medical signs]]
[[Category:Medical conditions related to obesity]]
[[Category:Diabetes]]
[[Category:Gross pathology]]
[[Category:Rehabilitation medicine]]
[[es:Atrofia muscular]]