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Eukaryon

Class Year

Chelsea Bueter 2007

Michelle McKinzey 2007

Chloe Salzmann 2007

Michael Zorniak 2007

Keywords

Skeletal Muscle Atrophy

Abstract

Skeletal Muscle Atrophy (SMA) is a phenomenon found in many diseases and disorders. SMA is characterized by protein degradation induced by various pathways. Ten years ago, little was known about the mechanisms that lead from these disorders to protein degradation. Current research focuses on the mechanisms thought to induce SMA. It is now known that many of these pathways involve ubiquitin conjugate accumulation and increased proteasome activity resulting in rapid protein degradation and decreased synthesis. HIV associated proteins, such as Vpr, cause overexpression of atrogin-1 which promotes atrophy. Cachexia operates mainly through the IKK/NF¨ºB pathway and MuRF-1 Ub-ligase overexpression causes SMA. In contrast, the onset of oxidative stress increases intracellular calcium levels, activating endoproteases and stimulating myofilament degradation. Lastly, diabetes acts in a similar way. Low insulin levels trigger ub-conjugation and proteasome activity leading to SMA. In order to treat SMA in the aforementioned disorders, specified inhibitor drugs are being considered for hindering the pathway. This review proposes to use the HIV virus as a model to investigate how these diseases induce SMA with further investigations of the mechanisms from HIV to the aforementioned diseases. Possible treatments are associated with the reverse pathway, hypertrophy, which suppresses protein degradation and increases synthesis.

Disclaimer

Eukaryon is published by students at Lake Forest College, who are solely responsible for its content. The views expressed in Eukaryon do not necessarily reflect those of the College. Articles published within Eukaryon should not be cited in bibliographies. Material contained herein should be treated as personal communication and should be cited as such only with the consent of the author.

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