Gynecology · Published 2025-06-17 · DOI 10.26442/20795696.2025.2.203308
Hyaluronic acid (HA) is a key component of the extracellular matrix involved in regulating inflammation, fibrosis, and tissue repair. Its biological properties depend on molecular weight: high-molecular-weight HA (HMW-HA) exhibits anti-inflammatory effects, whereas low-molecular-weight fragments (LMW-HA) induce inflammation and fibrosis by activating CD44, TLR, and RHAMM receptors. An imbalance between these forms may contribute to chronic inflammatory and fibrotic processes. HA metabolism is regulated by synthases (HAS) and hyaluronidases (HYAL). During chronic inflammation, HYAL-2 degrades HMW-HA into LMW-HA, which accumulates and sustains the inflammatory response. Native hyaluronidase preparations have limited efficacy due to rapid inactivation. Conjugation of the enzyme with azoximer enhances its resistance to inhibitors and proteases while prolonging its action. Bovhyaluronidase azoximer (Longidaza) breaks down pro-inflammatory LMW-HA into safe ultra-low-molecular-weight fragments, suppressing inflammation and fibrosis. The drug is active in the acidic environment of inflamed tissues without damaging healthy tissue. Its anti-fibrotic and anti-adhesive properties have been confirmed experimentally and clinically. Clinical studies demonstrate the drug’s efficacy in various fields: preventing postoperative adhesions, treating fibrotic changes in pulmonology, and correcting scars in dermatology. Thus, modulation of HA metabolism using conjugated hyaluronidase represents a promising approach for managing chronic inflammatory and fibrotic conditions.
Abstract from DOAJ. Public domain (CC0 1.0).
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