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The clinical conditions affecting the skeletal muscle tissue are broadly categorized as musculoskeletal and neuromuscular disorders.
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Alterations in Muscle Tone ll

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Alterations in muscle tone are common manifestations of neurological disorders and reflect dysfunction within different nervous system regions. Spasticity, paratonia, and dystonia represent distinct forms of hypertonia, each with unique mechanisms, clinical features, and diagnostic importance.CharacteristicsSpasticity happens from upper motor neuron lesions and is characterized by velocity-dependent resistance to passive movement. Clinical features include:Exaggerated deep tendon reflexesClonus...

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Related Experiment Video

Updated: May 24, 2026

Myo-mechanical Analysis of Isolated Skeletal Muscle

Myo-mechanical Analysis of Isolated Skeletal Muscle

Published on: February 22, 2011

TWEAK and TRAF6 regulate skeletal muscle atrophy.

Ashok Kumar¹, Shephali Bhatnagar, Pradyut K Paul

¹Department of Anatomical Sciences and Neurobiology, University of Louisville School of Medicine, Louisville, KY 40202, USA. ashok.kumar@louisville.edu

Current Opinion in Clinical Nutrition and Metabolic Care

|February 28, 2012

Summary

Tumor necrosis factor-like weak inducer of apoptosis (TWEAK) and TRAF6 are newly identified regulators of skeletal muscle atrophy. Targeting these proteins may offer future therapies for muscle wasting conditions.

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Area of Science:

Muscle physiology and molecular biology
Cell signaling pathways
Disease mechanisms

Background:

Proinflammatory cytokines contribute to muscle atrophy in chronic diseases.
The role of cytokines in disuse-induced muscle atrophy is emerging.
Signaling events triggering catabolic pathways in muscle atrophy require further understanding.

Purpose of the Study:

To elucidate the roles of TWEAK and TRAF6 in skeletal muscle atrophy.
To discuss the mechanisms of action of TWEAK and TRAF6 in muscle wasting.
To review current understanding of these proteins in atrophic conditions.

Main Methods:

Review of recent scientific literature on TWEAK, TRAF6, and skeletal muscle atrophy.
Analysis of signaling pathways involved in muscle catabolism.
Examination of experimental models of muscle wasting.

Main Results:

The TWEAK-Fn14 system is identified as a novel inducer of skeletal muscle wasting.
Atrophy conditions like denervation and unloading upregulate Fn14, activating TWEAK-mediated proteolytic pathways.
TRAF6 expression and activity increase in muscle atrophy models; its ablation prevents atrophy induction.

Conclusions:

TWEAK and TRAF6 are novel regulators of skeletal muscle atrophy.
These proteins represent potential molecular targets for preventing or treating muscle atrophy.
Further research into TWEAK and TRAF6 pathways could lead to new therapeutic strategies.