Therapeutic Induction of Heat Shock Proteins and the Potential Use as Treatment in Tendonitis
Kihoon Bohle
Introduction. Tendonitis is a broad term used to characterize inflammation of a tendon. It is one of the more common overuse injuries and is characterized by pain at the associated joint, stiffness, soreness, warmth, redness, and localized inflammation1. In response to cycles of tensile stress, tenocytes within the tendon respond to forces by secreting collagen fibers, anti-inflammatory mediators, and heat shock proteins, particularly HSP70. HSP70 is a family of heat shock proteins with effects ranging from tendon recovery to inflammation mediation4. While HSP70 exists in baseline as a normal physiological state, certain practices, habits, and therapies can induce HSP70 both in the short term and long term13. This abstract will analyze what lab and empirical evidence there is for the relationship between HSP70 and tendon injury prevention and recovery. It will also look at existing and novel ways to incorporate therapeutic practices that induce HSP70. Tendons naturally recover from wear and tear via signaling to tenocytes4. However, with overuse injuries, damaged tissue can buildup and lead to inflammation. This can lead to tendon adhesion, which is characterized as a disordered state of collagen fiber deposition leading to reduced mobility and pain7. Methods and Results HSP70 gene silencing has been correlated with worse tendon adhesion outcomes7. In another study, HSP70 levels were increased via photobiomodulation and similar results were found; increased collagen fiber deposition6. Additionally, HSP72, a protein within the HSP70 family, was upregulated to determine it’s relationship with fibroblast proliferation and tendon adhesion. Increased HSP72 levels in rats were linked with reduced fibroblast and collagen levels and subsequent better tendon adhesion scores8. Conclusion. There are multiple ways by which people can increase their HSP70 levels, including heat therapy, dietary changes, aerobic and anerobic exercise, fasting, and others3. However, this analysis focuses on heat therapy, both localized and systemic. Thermal pretreatment in rats for 15 minutes at 113°F was shown to increase HSP70 levels and reduce tendon adhesion post-recovery7. In humans, sauna sessions for 30 minutes at 163°F and localized heat therapy both increased HSP70 expression by at least 40% when compared to baseline14. HSP70 levels persisted beyond the short term with heat therapies. This research shows the potential that lies in inducing HSP70 to prevent tendon injury and increase recovery. It also highlights the need to reconsider current practices when it comes to therapies for managing tendonitis.
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