A New Way to Protect Muscle Degeneration

At a Glance

Researchers at Colorado State University have developed a promising drug-based treatment to prevent muscle loss in people who have limited mobility. The treatment uses specific compounds in the histone deacetylase (HDAC) inhibitor family to preserve muscle strength and structure. This new use of these HDACi compounds could offer new hope for patients confined to bed, wheelchairs, or astronauts in space! This approach may be more effective, accessible, and less labor-intensive than current therapies including physiotherapy.

Background

Disuse-induced muscle atrophy is a serious problem in people who are immobilized due to injury, illness, or extended inactivity, including astronauts in zero gravity. Traditional therapies such as physiotherapy can be costly, laborious, and not always effective. There is growing interest in molecular therapies that can act on the root biological causes of muscle degradation. HDAC inhibitors—compounds already known for gene regulation—offer a new way to treat this condition by modulating gene expression related to muscle preservation.

Overview

This novel therapy involves administering HDAC inhibitors to individuals at risk of muscle loss due to inactivity. These compounds work by selectively targeting specific HDAC classes (Class I, IIA, and IIB), which play a key role in regulating genes involved in muscle structure and function. By modulating gene expression, the treatment can prevent, slow, or even reverse the symptoms of disuse-induced muscular atrophy.

The approach has potential for broad use across human and animal patients, offering a proactive and less physically demanding alternative to traditional rehabilitation methods. Additionally, researchers have identified several biomarker genes—such as Fbxo32, TRIM63, and IGF1—whose expression is positively affected by the treatment. This enables more precise targeting and monitoring of the therapeutic effects at the molecular level.

Figure 1: H&E staining of hindlimb muscles revealed distinct structural differences between baseline and hindlimb unloaded (HU) conditions. Muscles from HU mice exhibited notable pathological features, including increased intracellular vacuolation and signs of lipid infiltration, indicative of muscle degeneration. In contrast, treatment with TSA mitigated these changes, restoring muscle histology toward the baseline phenotype with reduced vacuoles and preserved fiber integrity.

Benefits

Prevents or slows muscle loss without requiring physical activity
Targets gene expression directly to maintain muscle health
Potentially effective for both human and non-human patients
Applicable in a variety of clinical and non-clinical settings (e.g., spaceflight)
Reduces patient dependency on caregivers and physiotherapy services
Compatible with other treatment strategies

Applications

Treatment for bedridden or immobilized patients (e.g., cancer, injury, stroke)
Therapy for astronauts to prevent muscle wasting during long-term space missions
Veterinary use for animals with limited mobility
Adjunct to traditional rehabilitation in chronic conditions like fibromyalgia
Use in orthopedic recovery to preserve muscle during healing

Last Updated: July 2025

Opportunity

Available for Exclusive Licensing, Collaboration or Funding
TRL: 5

IP Status

US Provisional Patent

Inventors

Soham Ghosh
Kanita Hrustanovic

Reference Number

2025-031

Licensing Manager

Steve Foster
Steve.Foster@colostate.edu
970-491-7100