University of Pittsburgh researchers have discovered that metformin (Met), a commonly used medicine to treat type 2 diabetes, to promote soft tissue healing and prevent the development of fibrosis and resulting tendinopathy. Met can target the root cause of tendinopathy by promoting angiogenesis. As an FDA-approved compound, Met has the potential to be a safe, effective and economical option to treat age- and trauma-related tendinopathies.
Description
Tendinopathy, the inflammation and degradation of tendons, can be brought about by traumatic injury, overuse, or aging. It is a significant cause of disability for millions of Americans with cases expected to increase with the aging population. Within the US military alone, tendinopathies account for nearly 80% of musculoskeletal injuries in active-duty personnel, impacting on military readiness and resulting in billions of dollars in healthcare costs. Developing treatment strategies for soft tissue injuries that could avoid fibrosis development and subsequent tendinopathy has the potential to improve patient lives and save $billions in healthcare related costs.
Applications
• Tendinopathy prevention
• Tendinopathy treatment
• Soft tissue injury treatment with scar tissue reduction, including mild traumatic brain injury
Advantages
Current treatments for soft tissue injuries primarily focus on pain relief through nonsteroidal anti-inflammatory drugs (NSAIDs) corticosteroid injections, and the RICE (Rest, Ice, Compression, Elevation). However, these do not address the the root cause: the presence of high mobility group box 1 (HMGB1) protein during the inflammatory stage of soft tissue healing. HMGB1 can lead to varying degrees of fibrosis, particularly in tendons.
Metformin can inhibit HMGB1 and target downstream inflammatory agents including COX/PGE1, IL-1, and IL-6. Additionally, metformin promotes angiogenesis which can reduce healing time and lead to enhanced tissue healing with high-quality tissue regeneration.
Invention Readiness
In vivo studies in mice with Achilles tendon injuries treated with intraperitoneal injections of metformin demonstrated that the treatment increased and activated AMPK while suppressing TGF-β1 levels within the healing tendon in acute injuries. Tendon healing was further improved by blocking the migration of α-SMA+ myofibroblasts, which reduced the prevalence of disorganized collagen fibers and collagen type III. Additionally, treatment of tendons in aging mice with metformin resulted in decreased expression of inflammatory markers and improved tendon structure, suggesting that metformin t could be a potential treatment for both acute and chronic tendinopathies.
IP Status
Patent Pending
